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.

Studies have recorded an incidence of about 3–5 cases per 1,000 newborn babies.

Experts, such as the American Academy of Dermatology, say that vast majority of moles are benign. Nonetheless, the U.S. National Cancer Institute estimated that 62,480 new cases of melanoma and 8,420 related deaths would appear in the United States in the year 2008.

Data on the chances of transformation from melanocytic nevi to melanoma is controversial, but it appears that about 10% of malignant melanomas have a precursor lesion, of which about 10% are melanocytic nevi. Therefore, it appears that malignant melanoma quite seldomly (1% of cases) has a melanocytic nevi as a precursor.

Halo nevi are estimated to be present in approximately 1% of the general population, and are found to be more prevalent in people with vitiligo, malignant melanoma, or Turner syndrome. All races and sexes are equally susceptible to this disease, although a familial tendency has been reported. The average age of onset is in a person's teenage years.

Nevus depigmentosus or nevus achromicus is a loss of pigment in the skin which can be easily differentiated from vitiligo. Although age factor has not much involvement in the nevus depigmentosus but in about 19% of the cases these are noted at birth. Their size may however grow in proportion to growth of the body. The distribution is also fairly stable and are nonprogressive hypopigmented patches. The exact cause of nevus depigmentosus is still not clearly understood. A sporadic defect in the embryonic development has been suggested to be a causative factor.

It has been described as "localised albinism", though this is incorrect. Those with nevus depigmentosus may be prone to sunburn due to the lack of pigment, and the patient should use good sun protection. Sunscreen should be applied to all exposed skin, since reduced tanning of normal skin will decrease the contrast with hypopigmented skin. Most patients with nevus depigmentosus do not pursue treatment for their lesion. There is no way to repigment the skin. If, however, the lesion is of cosmetic concern, camouflage makeup is effective. If the lesion is small one could also consider excision.

These are localized white spots on skin which may affect any area of the body, but these white spots are quite stable lesions. In the majority of patients, the lesions are not completely achromic, but are hypopigmented and resemble splashed paint. The individual lesions are permanent and there are no effective therapies for re-pigmenting this nevus. If there is hair in an affected area, it is usually colourless or white.

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.

Usually observed at birth or shortly thereafter in 94% of patients, in other reports, patients did not develop skin lesions until 3 months or even 2 years after birth. Females are typically affected more often than males (64%).

Café au lait spots can arise from diverse and unrelated causes:

- Having six or more café au lait spots greater than 5 mm in diameter before puberty, or greater than 15 mm in diameter after puberty, is a diagnostic feature of neurofibromatosis type I, but other features are required to diagnose NF-1.

- Familial multiple café au lait spots have been observed without NF-1 diagnosis.

- They can be caused by vitiligo in the rare McCune–Albright syndrome.

- Legius syndrome

- Tuberous sclerosis

- Fanconi anemia

- Idiopathic

- Ataxia-telangiectasia

- Basal cell nevus syndrome

- Benign congenital skin lesion

- Bloom syndrome

- Chédiak–Higashi syndrome

- Congenital naevus

- Gaucher disease

- Hunter syndrome

- Jaffe–Campanacci syndrome

- Maffucci syndrome

- Multiple mucosal neuroma syndrome

- Noonan syndrome

- Pulmonary Stenosis

- Silver–Russell syndrome

- Watson syndrome

- Wiskott–Aldrich syndrome

Medical knowledge and documentation of this disorder is poor, likely due to a combination of factors including recent discovery, low prevalence, and the more or less aesthetic nature of the effects of the skin disorder. Thus the pathophysiology of Becker's nevus remains unclear. While it is generally considered an acquired rather than congenital disorder, there exists at least one case report documenting what researchers claim is a congenital Becker's nevus with genetic association: a 16-month-old boy with a hyperpigmented lesion on his right shoulder whose father has a similar lesion on his right shoulder.

The most extensive study to date, a 1981 survey of nearly 20,000 French males aged 17 to 26, served to disprove many commonly held beliefs about the disorder. In the French study, 100 subjects were found to have Becker's nevi, revealing a prevalence of 0.52%. Nevi appeared in one half the subjects before the age of 10, and between ages 10 and 20 in the rest. In one quarter of cases sun exposure seems to have played a role, a number apparently lower than that expected by researchers. Also surprising to researchers was the low incidence (32%) of Becker's nevi above the nipples, for it had generally been believed that the upper chest and shoulder area was the predominant site of occurrence. Pigmentation was light brown in 75% of cases (note: subjects were Caucasian), and average size of the nevus was 125 cm² (19 in²).

The prognosis is favorable in most patients with an isolated cutaneous abnormality. In the majority of cases, both the vivid red marking and the difference in circumference of the extremities regress spontaneously during the first year of life. It is theorized that this may be due to the normal maturation process, with thickening of the epidermis and dermis. Improvements for some patients can continue for up to 10 years, while in other cases, the marbled skin may persist for the patient's lifetime.

One study reported an improvement in lesions in 46% of patients within 3 years. If CMTC persists into adulthood, it can result in complaints due to paresthesia, increased sensitivity to cold and pain, and the formation of ulcers.

Few reports included long-term follow up of CMTC into adolescence and adulthood. While about 50% of patients seem to show definite improvement in the reticular vascular pattern, the exact incidence and cause of persistent cases are unknown.

Large and especially giant congenital nevi are at higher risk for malignancy degeneration into melanoma. Because of the premalignant potential, it is an acceptable clinical practice to remove congenital nevi electively in all patients and relieve the nevocytic overload.

These nevi represent excess growth of blood vessels, including capillaries.

- Nevus simplex (also known as a stork bite, salmon patch, or Nevus flammeus neonatorum)

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.

As halo nevi are only of cosmetic significance, no treatment is required, and patients will be asymptomatic. Although halo nevi are harmless, it is important to monitor the lesion on regular basis. Watch out for any changes in appearance of existing or new halo nevi. If there is any change in appearance or is associated with pain, itch, and infection, a doctor should be consulted immediately to exclude the possibility of melanoma.

A 1991 report documented the cases of nine patients with both Becker's nevus and malignant melanoma. Of the nine melanomas, five were in the same body area as the Becker's nevus, with only one occurring within the nevus itself. As this was apparently the first documented co-occurrence of the two diseases, there is so far no evidence of higher malignancy rates in Becker's nevi versus normal skin. Nonetheless, as with any abnormal skin growth, the nevus should be monitored regularly and any sudden changes in appearance brought to the attention of one's doctor.

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.

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

Port-wine stains were shown to be caused by a somatic activating c.548G→A mutation in the GNAQ gene. An association with RASA1 has also been described.

Nevus anemicus is a congenital disorder characterized by macules of varying size and shape that are paler than the surrounding skin and cannot be made red by trauma, cold, or heat. The paler area is due to the blood vessels within the area which are more sensitive to the body’s normal vasoconstricting chemicals.

Spitz nevi are uncommon. Their annual incidence was estimated in a coastal population of sub-tropical Queensland to be 1.4 cases per 100,000 people. For comparison, the annual incidence of melanoma in the same population, which is high by world standards is 25.4 cases per 100,000 people.

Although they are most commonly found on people in their first two decades of life, the age range for people with Spitz nevi is from 6 months to 71 years, with a mean age of 22 years and a median age of 19 years.

Nevoid melanoma is a cutaneous condition that may resemble a Spitz nevus or an acquired or congenital melanocytic nevus.

This benign patch appears on the skin at birth or in early childhood. In most people these are under 10cm in size. If there is doubt about the diagnosis, rubbing the area causes the skin around the lesion to become red while the lesion itself does not change in color. Often the patches are difficult to see against the background color of the patient’s skin, but if sunburn develops, then the white area stands out prominently. The involved area is lighter than the normal skin, not because of a loss of pigment occurs, but because blood vessels are constricted, producing a permanent blanching of the area. This blanching is a functional rather than a structural abnormality, presumed to be caused by local increased sensitivity to catecholamines. Although the cutaneous vasculature appears normal histologically, the blood vessels within the nevus do not respond to injection of vasodilators. It has been postulated that the persistent pallor may represent a sustained localized adrenergic vasoconstriction. Results of a skin biopsy would be interpreted as normal and only physiological testing can reveal the nevus in contrast to normal skin. Stroking the patch elicits no red flare. Only the normal skin would react with a characteristic erythematous response. Examination under a Wood lamp can also reveal the nevus anemicus patch will not emphasize as a patch of vitiligo would.

Linear verrucous epidermal nevus (also known as a "Linear epidermal nevus," and "Verrucous epidermal nevus") is a skin lesion characterized by a verrucous skin-colored, dirty-gray or brown papule. Generally, multiple papules present simultaneously, and coalesce to form a serpiginous plaque. When this nevus covers a diffuse or extensive portion of the body's surface area, it may be referred to as a systematized epidermal nevus, when it involved only one-half of the body it is called a nevus unius lateris.

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.