Mongolian spots usually resolve by early childhood and hence no treatment is generally needed if they are located in the sacral area. However, sometimes it may be required for extra sacral lesions to have surgical correction. Q-switched alexandrite lasers have been used for treatment. Good results are obtained if treatment is initiated before the age of 20 years. In a study done by the University of Tokyo, the effectiveness of the Q-switched alexandrite laser in treating Mongolian spots was evaluated. A retrospective study was done from April 2003 to September 2011. 16 patients, aged 14-55, were treated with Q-switched alexandrite laser. A good therapeutic outcome was achieved on the whole group, however two patients with sacral Mongolian spots suffered from inflammatory hyperpigmentation, and two patients got post inflammatory hypopigmentation after seven sessions of laser treatment.

Males and Females get Mongolian spots equally. A hospital-based, cross-sectional, prospective study was conducted in the Department of Dermatology, Venereology and Leprosy, BLDE University, Shri B. M. Patil Medical College Hospital and Research Center, Bijapur. One thousand neonates delivered in the Department of Obstetrics and Gynecology of the same institution was surveyed for the presence of skin lesions. The study was conducted in the period of November 2007 to May 2009. The study showed that 467 males were born with Mongolian spots and 380 females were born with Mongolian spots. The results showed there was no statistical significance in males and females born with Mongolian spots. Within the same study, different racial groups were recorded and documented. The study showed that among the Australian neonate, 25.5% were born with Mongolian spots. In the Iranian neonate, 71-81% were reported, in the Japanese neonate 81.5%, in the Turkish neonate 13.2%, in the caucasian neonate 62.8%, in the African American neonate 86.6%, and in the Indian neonate 72-89% were reported in having Mongolian spots. The populations with the most incidences of Mongolian spots were Iranian, Japanese, African American, and Indian.

A Q-switched laser has been successfully used to treat the condition.

Most birthmarks are harmless and do not require treatment. Pigmented marks can resolve on their own over time in some cases. Vascular birthmarks may require reduction or removal for cosmetic reasons. Treatments include administering oral or injected steroids, dermatological lasers to reduce size and/or color, or dermatologic surgery.

Liver spots (also known as age spot, solar lentigo, "lentigo senilis", "old age spot", "senile freckle") are es on the skin associated with aging and exposure to ultraviolet radiation from the sun. They range in color from light brown to red or black and are located in areas most often exposed to the sun, particularly the hands, face, shoulders, arms and forehead, and the scalp if bald.

The spots derive their name from the fact that they were once incorrectly believed to be caused by liver problems, but they are physiologically unrelated to the liver, save for a similar color. From the age of 40 onward the skin is less able to regenerate from sun exposure, and liver spots are very common in this age group, particularly in those who spend time in the sun.

In the overwhelming majority of cases, liver spots pose no threat and require no treatment, though they occasionally have been known to obscure the detection of skin cancer. However, despite being a benign condition, liver spots are sometimes considered unsightly and some people choose to have them removed. This can be done by electrosurgery, laser treatment, cryotherapy, or the use of depigmentation agents, such as hydroquinone, tretinoin, topical cysteamine, azelaic acid or alpha hydroxy acids.

Café au lait spots can be removed with lasers. Results are variable as the spots are often not completely removed or can come back after treatment. Often, a test spot is treated first to help predict the likelihood of treatment success.

Differently from the melanotic nevi and the verrucous nevi on the skin, age spots change with time in color and in shape. Misrepair-accumulation aging theory proposes a hypothesis on the development of age spots. Firstly, the development of a flat spot is a result of accumulation of aged basal cells. When the skin is aged, some aged cells that contain lipofuscin bodies cannot be removed. An aged cell will affect the functionality of the local tissue and promote the aging of its neighbor cells. By a feedback loop, more and more neighbor cells become aged and lipofuscin-containing. They aggregate and form a spot with an irregular shape. Secondly, protruding of a flat spot is a result of the death of aged cells in the spot and release of lipofuscin bodies. Isolation of the un-digestible lipofuscin bodies in a fibrotic capsule is essential for maintaining the structural integrity of the tissue. Successive encapsulation of dead cells and lipofuscin bodies results in the growth of a spot in three dimensions. The dense lipofuscin bodies in the capsule make a protruding spot soft and dark in color.

Nevus of Ota (also known as "congenital melanosis bulbi", "nevus fuscoceruleus ophthalmomaxillaris", "oculodermal melanocytosis", and "oculomucodermal melanocytosis") is a blue hyperpigmentation that occurs on the face. It was first reported by Dr. M.T. Ota of Japan in 1939.

Nevus of Ota is caused by the entrapment of melanocytes in the upper third of the dermis. It is found on the face unilaterally and involves the first two branches of the trigeminal nerve. The sclera is involved in two-thirds of cases (causing an increased risk of glaucoma). It should not be confused with Mongolian spot, which is a birthmark caused by entrapment of melanocytes in the dermis but is located in the lumbosacral region. Women are nearly five times more likely to be affected than men, and it is rare among Caucasian people. Nevus of Ota may not be congenital, and may appear during puberty.

In season 6 of House MD in the episode 12 titled Remorse, House diagnoses his patient with Wilson's Disease in absence of Kayser-Fleischer rings by removing the nail polish to note the blue nails.

Mole removal risks mainly depend on the type of mole removal method the patient undergoes. First, mole removal may be followed by some discomfort that can be relieved with pain medication. Second, there is a risk that a scab will form or that redness will occur. However, such scabs and redness usually heal within one or two weeks. Third, as in other surgeries, there is also risk of infection or an anesthetic allergy or even nerve damage. Lastly, the mole removal may imply an uncomfortable scar depending on the mole size.

A birthmark is a congenital, benign irregularity on the skin which is present at birth or appears shortly after birth, usually in the first month. They can occur anywhere on the skin. Birthmarks are caused by overgrowth of blood vessels, melanocytes, smooth muscle, fat, fibroblasts, or keratinocytes.

Dermatologists divide birthmarks into two types. Pigmented birthmarks caused by excess skin pigment cells include moles, café au lait spots, and Mongolian spots. Vascular birthmarks, also called red birthmarks, are caused by increased blood vessels and include macular stains (salmon patches), hemangiomas, and Port-wine stains. A little over 1 in 10 babies have a vascular birthmark present by age 1. Several birthmark types are part of the group of skin lesions known as nevi or naevi, which means "birthmarks" in Latin.

The exact cause of most birthmarks is unknown, but they are thought to occur as a result of a localized imbalance in factors controlling the development and migration of skin cells. In addition, it is known that vascular birthmarks are not hereditary.

Ultraviolet light from the sun causes premature aging of the skin and skin damage that can lead to melanoma. Some scientists hypothesize that overexposure to UV, including excessive sunlight, may play a role in the formation of acquired moles. However, more research is needed to determine the complex interaction between genetic makeup and overall exposure to ultraviolet light. Some strong indications that this is so (but falling short of proof), are:

- The relative lack of moles on the buttocks of people with dysplastic nevi.

- Freckles (spots of melanin on the skin, and distinct from moles) are known to be influenced by sunlight.

Studies have found that sunburns and too much time in the sun can increase the risk factors for melanoma. This is "in addition to" those who have dysplastic nevi being at higher risk of this cancer (the uncertainty is in regard to acquiring "benign" moles). To prevent and reduce the risk of melanoma caused by UV radiation, the American Academy of Dermatology and the National Cancer Institute recommends staying out of the sun between 10 a.m. and 4 p.m. standard time (or whenever one's shadow is shorter than one's height). The National Cancer Institute also recommends wearing long sleeves and trousers, hats with a wide brim, sunscreens, and sunglasses that have UV-deflecting lenses.

Blue nails, or more formally azure lunula, are characterized by a blue discoloration of the lunulae, seen in argyria and cases of hepatolenticular degeneration (Wilson's disease), also having been reported in hemoglobin M disease and hereditary acrolabial telangiectases.

In Wilson's disease the blue color involves the lunula (most intense pigmentation) and fades proximally. In argyria, the nail is permanently pigmented a slate-blue color and is most evident in the lunula. Minocycline and Zidovudine can also turn the nail plate blue-gray. There are also reports of hydroxyurea as a rare cause.

Café au lait" spots or café au lait" macules are flat, pigmented birthmarks. The name "café au lait" is French for "coffee with milk" and refers to their light-brown color. They are also called "giraffe spots" or "coast of Maine spots".

They are caused by a collection of pigment-producing melanocytes in the epidermis of the skin.

These spots are typically permanent, and may grow or increase in number over time.

Café au lait spots are often harmless, but may be associated with syndromes such as neurofibromatosis type 1 and McCune–Albright syndrome.

The decision to observe or treat a nevus may depend on a number of factors, including cosmetic concerns, irritative symptoms (e.g., pruritus), ulceration, infection, and concern for potential malignancy.

Lethal white syndrome (LWS), also called overo lethal white syndrome (OLWS), lethal white overo (LWO), and overo lethal white foal syndrome (OLWFS), is an autosomal genetic disorder most prevalent in the American Paint Horse. Affected foals are born after the full 11-month gestation and externally appear normal, though they have all-white or nearly all-white coats and blue eyes. However, internally, these foals have a nonfunctioning colon. Within a few hours, signs of colic appear; affected foals die within a few days. Because the death is often painful, such foals often are humanely euthanized once identified. The disease is particularly devastating because foals are born seemingly healthy after being carried to full term.

The disease has a similar cause to Hirschsprung's disease in humans. A mutation in the middle of the endothelin receptor type B (EDNRB) gene causes lethal white syndrome when homozygous. Carriers, which are heterozygous—that is, have one copy of the mutated allele, but themselves are healthy—can now be reliably identified with a DNA test. Both parents must be carriers of one copy of the LWS allele for an affected foal to be born.

Horses that are heterozygous for the gene that causes lethal white syndrome often exhibit a spotted coat color pattern commonly known as "frame" or "frame overo". Coat color alone does not always indicate the presence of LWS or carrier status, however. The frame pattern may be minimally expressed or masked by other spotting patterns. Also, different genetic mechanisms produce healthy white foals and have no connection to LWS, another reason for genetic testing of potential breeding stock. Some confusion also occurs because the term overo is used to describe a number of other non tobiano spotting patterns besides the frame pattern. Though no treatment or cure for LWS foals is known, a white foal without LWS that appears ill may have a treatable condition.

Not all white, blue-eyed foals are affected with LWS. Other genes can produce healthy pink-skinned, blue-eyed horses with a white or very light cream-colored coat. For a time, some of these completely white horses were called "living lethals", but this is a misnomer. Before reliable information and the DNA test were available to breeders, perfectly healthy, white-coated, blue-eyed foals were sometimes euthanized for fear they were lethal whites, an outcome which can be avoided today with testing and a better understanding of coat color genetics or even waiting 12 hours or so for the foal to develop clinical signs. The availability of testing also allows a breeder to determine if a white-coated, blue-eyed foal that becomes ill is an LWS foal that requires euthanasia or a non-LWS foal with a simple illness that may be successfully treated.

- Double-cream dilutes such as cremello, perlinos, and smoky creams, have cream-colored coats, blue eyes, and pink skin. The faint cream pigmentation of their coats can be distinguished from the unpigmented white markings and underlying unpigmented pink skin. A similar-looking "pseudo double dilute" can be produced with help from the pearl gene or "barlink factor" or the champagne gene.

- The combination of tobiano with other white spotting patterns can produce white or nearly white horses, which may have blue eyes.

- Sabino horses that are homozygous for the sabino-1 ("Sb-1") gene are often called "sabino-white", and are all- or nearly all-white. Not all sabino horses carry "Sb-1".

- Dominant white genetics are not thoroughly understood, but are characterized by all- or nearly all-white coats.

Heterochromia has also been observed in those with Duane syndrome.

Acquired heterochromia is usually due to injury, inflammation, the use of certain eyedrops that damages the iris, or tumors.

The management of a nevus depends on the specific diagnosis, however, the options for treatment generally include the following modalities:

Daentl Townsend Siegel syndrome is a very rare disorder characterized by blue sclerae, kidney malfunction, thin skin, and hydrocephalus. It was first identified by D.L. Daentl et al. in 1978. Daentl Townsend Siegel syndrome is also known as "Hydrocephalus blue sclera nephropathy" and "Familial nephrosis, hydrocephalus, thin skin, blue sclerae syndrome".

The odd-eyed coloring is caused when either the epistatic (dominant) white gene (which masks any other color genes and turns a cat completely white) or the white spotting gene (which is the gene responsible for bicolor and tuxedo cats) prevents melanin (pigment) granules from reaching one eye during development, resulting in a cat with one blue eye and one green, yellow, or brown eye. The condition only rarely occurs in cats that lack both the dominant white and the white spotting gene.

Blue nevus (also known as "blue neuronevus", "dermal melanocytoma", and "nevus bleu") is a type of melanocytic nevus. The blue colour is caused by the pigment being deeper in the skin than in ordinary nevi. In principle they are harmless but they can sometimes be mimicked by malignant lesions, i.e. some melanomas can look like a blue nevus.

As with some newborn mammals, all cats are blue-eyed as kittens, and may change as the newborn ages. The differences in an odd-eyed kitten's eye color might not be noticeable, save upon close inspection. Odd-eyed kittens have a different shade of blue in each eye. The color of the odd eye changes over a period of months–for example, from blue to green to yellow or from green to blue to yellow–until it reaches its final, adult color.

Microcoria is a congenital disease in which the pupils of the subject are narrower than 2 mm in diameter. Microcoria is associated with juvenile-onset glaucoma. It is also associated with Pierson syndrome chararacterized by microcoria and congenital nephrotic syndrome. The defect is in the Laminin beta 2 gene on chromosome 3p21 which encodes a protein essential to the glomerular basement membrane.

It is also part of the known manifestations of a born infant to a mother suffering from uncontrolled hyperglycemia. Other symptoms include transposition of great vessels, respiratory distress secondary to surfactant defect, sacral agensis, jitteriness, irritability, and lethargy due to rebound fetal hypoglycemia. Congenital microcoria is an autosomal dominant trait. However, it can also occur sporadically.