An estimated 20 per million live births are diagnosed with EB, and 9 per million people in the general population have the condition. Of these cases, approximately 92% are epidermolysis bullosa simplex (EBS), 5% are dystrophic epidermolysis bullosa (DEB), 1% are junctional epidermolysis bullosa (JEB), and 2% are unclassified. Carrier frequency ranges from 1 in 333 for JEB, to 1 in 450 for DEB; the carrier frequency for EBS is presumed to be much higher than JEB or DEB.

The disorder occurs in every racial and ethnic group and affects both sexes.

IBS is an autosomal dominant genetic condition caused by a mutation in the gene for keratin 2e on chromosome 12.

This means an affected person has a 50% chance of passing the condition on to their child. Around half of cases of IBS, however, have no parent with the condition and have the genetic fault due to a spontaneous mutation.

A 2014 study classified cases into three types—epidermolysis bullosa simplex (EBS), junctional epidermolysis bullosa (JEB), and dystrophic epidermolysis bullosa (DEB) -- and reviewed their times of death. The first two types tended to die in infancy and the last in early adulthood.

Ichthyosis vulgaris is one of the most common genetic disorders caused by a single gene. The disorder is believed to be caused by mutations to the gene encoding profilaggrin (a protein which is converted to filaggrin which plays a vital role in the structure of the skin). Around 10% of the population have some detrimental mutations to the profilaggrin gene that is also linked to atopic dermatitis (another skin disorder that is often present with ichthyosis vulgaris). The exact mutation is only known for some cases of ichthyosis vulgaris.

It is generally considered to be an autosomal dominant condition, i.e., a single genetic mutation causes the disease and an affected person has a 50% chance of passing the condition on to their child. There is some research indicating it may be semi-dominant. This means that a single mutation would cause a mild case of ichthyosis vulgaris and mutations to both copies of the gene would produce a more severe case.

Ichthyosis bullosa of Siemens is a type of familial, autosomal dominant ichthyosis, a rare skin disorder. It is also known as bullous congenital ichthyosiform erythroderma of Siemens or ichthyosis exfoliativa. It is a genetic disorder with no known cure which is estimated to affect about 1 in 500,000 people.

Lichen sclerosus may have a genetic component. Higher rates of lichen sclerosus have been reported among twins and among family members.

Darier disease is inherited in an autosomal dominant manner, which indicates that the defective gene responsible for a disorder is located on an autosome, and only one copy of the gene is sufficient to cause the disorder, when inherited from a parent who has the disorder.

The disorder is caused by a mutation in the gene ATP2A2. Family members with confirmed identical ATP2A2 mutations can exhibit differences in the clinical severity of disease, suggesting that other genes or environmental factors affect the expression of Darier's disease. With the discovery of the ATP2A2 gene, performing genetic tests to confirm the diagnosis of Darier's disease is now possible.

A 1992 study of 163 affected persons found that most patients had no other medical problems and most manage to lead a relatively normal life.

Epidermolytic ichthyosis (EI), (also known as "epidermolytic hyperkeratosis (EHK)", "bullous congenital ichthyosiform erythroderma (BCIE), bullous ichthyosiform erythroderma, or bullous congenital ichthyosiform erythroderma Brocq) is a rare and severe form of ichthyosis this skin disease affects around 1 in 300,000 people.

It involves the clumping of keratin filaments.

Epidermolysis bullosa dystrophica or dystrophic EB (DEB) is an inherited disease affecting the skin and other organs.

"Butterfly child" is the colloquial name for a child born with the disease, as their skin is seen to be as delicate and fragile as that of a butterfly.

Although it is not clear what causes LS, several theories have been postulated. Lichen Sclerosus is not contagious; it cannot be caught from another person.

Several risk factors have been proposed, including autoimmune diseases, infections and genetic predisposition. There is evidence that LS can be associated with thyroid disease.

Topical steroid preparations often help outbreaks; use of the weakest corticosteroid that is effective is recommended to help prevent thinning of the skin. Drugs such as antibiotics, antifungals, corticosteroids, dapsone, methotrexate, thalidomide, etretinate, cyclosporine and, most recently, intramuscular alefacept may control the disease but are ineffective for severe chronic or relapsing forms of the disease. Intracutaneous injections of botulinum toxin to inhibit perspiration may be of benefit. Maintaining a healthy weight, avoiding heat and friction of affected areas, and keeping the area clean and dry may help prevent flares.

Some have found relief in laser resurfacing that burns off the top layer of the epidermis, allowing healthy non-affected skin to regrow in its place.

Secondary bacterial, fungal and/or viral infections are common and may exacerbate an outbreak. Some people have found that outbreaks are triggered by certain foods, hormone cycles and stress.

In a few cases naltrexone appears to help.

Ichthyosis vulgaris (also known as "Autosomal dominant ichthyosis," and "Ichthyosis simplex") is a skin disorder causing dry, scaly skin. It is the most common form of ichthyosis, affecting around 1 in 250 people. For this reason it is known as common ichthyosis. It is usually an autosomal dominant inherited disease (often associated with filaggrin), although a rare non-heritable version called acquired ichthyosis exists.

It is possible to classify epidermolytic hyperkeratosis based upon palm and sole hyperkeratosis.

This is a dominant genetic condition caused by mutations in the genes encoding the proteins keratin 1 or keratin 10.

- Keratin 1 is associated with the variants affecting the palms and soles.

- Keratin 10 is associated with the variants in which these are unaffected.

Urbach–Wiethe disease is very rare; there are fewer than 300 reported cases in medical literature. Although Urbach–Wiethe disease can be found worldwide, almost a quarter of reported diagnoses are in South Africa. Many of these are in patients of Dutch, German, and Khoisan ancestry. This high frequency is thought to be due to the founder effect. Due to its recessive genetic cause and the ability to be a carrier of the disease without symptoms, Urbach–Wiethe disease often runs in families. In some regions of South Africa, up to one in 12 individuals may be carriers of the disease. Most of the case studies involving Urbach–Wiethe disease patients involve only one to three cases and these cases are often in the same family. Due to its low incidence, it is difficult to find a large enough number of cases to adequately study the disease.

Congenital Ichthyosiform Erythroderma (CIE), also known as Nonbullous congenital ichthyosiform erythroderma is a rare type the ichthyosis family of skin diseases which occurs in 1 in 200,000 to 300,000 births.

While the term pemphigus typically refers to "a rare group of blistering autoimmune diseases" affecting "the skin and mucous membranes", Hailey–Hailey disease is not an autoimmune disorder and there are no autoantibodies. According to Pemphigus Pemphigoid Foundation (IPPF), "familial benign chronic pemphigus, or Hailey-Hailey disease, is a different condition from Pemphigus".

There are many types of ichthyoses and an exact diagnosis may be difficult. Types of ichthyoses are classified by their appearance and their genetic cause. Ichthyosis caused by the same gene can vary considerably in severity and symptoms. Some ichthyoses do not appear to fit exactly into any one type. Different genes can produce ichthyoses with similar symptoms. Of note, X-linked ichthyosis is associated with Kallmann syndrome (close to "KAL1" gene). The most common or well-known types are as follows:

The deficiency in anchoring fibrils impairs the adherence between the epidermis and the underlying dermis. The skin of DEB patients is thus highly susceptible to severe blistering.Collagen VII is also associated with the epithelium of the esophageal lining, and DEB patients may suffer from chronic scarring, webbing, and obstruction of the esophagus. Affected individuals are often severely malnourished due to trauma to the oral and esophageal mucosa and require feeding tubes for nutrition. They also suffer from iron-deficiency anemia of uncertain origin, which leads to chronic fatigue.

Open wounds on the skin heal slowly or not at all, often scarring extensively, and are particularly susceptible to infection. Many individuals bathe in a bleach and water mixture to fight off these infectionsThe chronic inflammation leads to errors in the DNA of the affected skin cells, which in turn causes squamous cell carcinoma (SCC). The majority of these patients die before the age of 30, either of SCC or complications related to DEB.

The chronic inflammatory state seen in recessive dystrophic epidermolysis bullosa (RDEB) may cause Small fiber peripheral neuropathy (SFN).; RDEB patients have reported the sensation of pain in line with neuropathic pain qualities.

Hyperpigmentation can be caused by sun damage, inflammation, or other skin injuries, including those related to acne vulgaris. People with darker skin tones are more prone to hyperpigmentation, especially with excess sun exposure.

Many forms of hyperpigmentation are caused by an excess production of melanin. Hyperpigmentation can be diffuse or focal, affecting such areas as the face and the back of the hands. Melanin is produced by melanocytes at the lower layer of the epidermis. Melanin is a class of pigment responsible for producing colour in the body in places such as the eyes, skin, and hair. As the body ages, melanocyte distribution becomes less diffuse and its regulation less controlled by the body. UV light stimulates melanocyte activity, and where concentration of the cells is greater, hyperpigmentation occurs. Another form of hyperpigmentation is post inflammatory hyperpigmentation. These are dark and discoloured spots that appear on the skin following acne that has healed.

Hyperpigmentation is associated with a number of diseases or conditions, including the following:

- Addison's disease and other sources of adrenal insufficiency, in which hormones that stimulate melanin synthesis, such as melanocyte-stimulating hormone (MSH), are frequently elevated.

- Cushing's disease or other excessive adrenocorticotropic hormone (ACTH) production, because MSH production is a byproduct of ACTH synthesis from proopiomelanocortin (POMC).

- Acanthosis nigricans—hyperpigmentation of intertriginous areas associated with insulin resistance.

- Melasma, also known as "chloasma"—patchy hyperpigmentation

- Acne scarring from post-inflammatary hyperpigmentation

- Linea nigra—a hyperpigmented line found on the abdomen during pregnancy.

- Peutz-Jeghers syndrome—an autosomal dominant disorder characterized by hyperpigmented macules on the lips and oral mucosa and gastrointestinal polyps.

- Exposure to certain chemicals such as salicylic acid, bleomycin, and cisplatin.

- Smoker's melanosis

- Coeliac disease

- Cronkite-Canada syndrome

- Porphyria

- Tinea fungal infections such as ringworm

- Haemochromatosis—a common but debilitating genetic disorder characterized by the chronic accumulation of iron in the body.

- Mercury poisoning—particularly cases of cutaneous exposure resulting from the topical application of mercurial ointments or skin-whitening creams.

- Aromatase deficiency

- Nelson's syndrome

- Grave's disease

- As a result of tinea cruris.

Hyperpigmentation can sometimes be induced by dermatological laser procedures.

Most patients with hyper IgE syndrome are treated with long-term antibiotic therapy to prevent staphylococcal infections. Good skin care is also important in patients with hyper IgE syndrome. High-dose intravenous gamma-globulin has also been suggested for the treatment of severe eczema in patients with HIES and atopic dermatitis.

Ichthyosis is a family of rare genetic skin disorders characterized by dry, thickened, scaly skin.

There are more than 20 types of ichthyosis which range in severity of symptoms, outward appearance, underlying genetic cause, and mode of inheritance (e.g., whether the abnormal gene inherited is dominant, recessive, autosomal, or X-linked). Ichthyosis comes from the , since dry, scaly skin is the defining feature of all forms of ichthyosis.

The severity of symptoms can vary enormously, from the mildest, most common, type such as ichthyosis vulgaris which may be mistaken for normal dry skin up to life-threatening conditions such as harlequin type ichthyosis. Ichthyosis vulgaris accounts for more than 95% of cases.

One of the biggest risks factors faced by the affected foals is susceptibility to secondary infection. Within three to eight days after birth, the foal may die from infection or is euthanized for welfare reasons.

Oudtshoorn is a town in Western Cape (formerly Cape Province), South Africa, where KWE ("Oudtshoorn skin") was first described. The disorder is quite prevalent among Afrikaners of South Africa, a population which can be defined as caucasoid native-speakers of Afrikaans, with northwestern European lineage. Among this group, KWE occurs at a rate of approximately 1/7,200.

This relatively high rate of occurrence has been attributed to the founder effect, in which a small, often consanguinous population is formed out of the larger ancestral population, resulting in a loss of genetic diversity. In the context of KWE, the founder effect was confirmed by haplotype analysis, which indicates that the chromosomal origin of a possible genetic mutation responsible for the disorder is particularly common among affected Afrikaners. This is also true in other South Africans of European descent with KWE, and the chromosome of interest in both these and Afrikaner patients strongly points to an unspecified ancestor or ancestral group that may have settled around the Oudtshoorn area.

A second lineage known to exhibit KWE has been reported in Germany, although there it is less prevalent and appears to involve the chromosome from a different ancestral origin than that seen in Afrikaners. KWE has also been noted in other countries around the northwestern region of Europe, such as Denmark.

Skin tags are thought to occur from skin rubbing up against skin, since they are so often found in skin creases and folds. Studies have shown existence of low-risk HPV 6 and 11 in skin tags, hinting at a possible role in its pathogenesis. Acrochorda have been reported to have a prevalence of 46% in the general population. A causal genetic component is thought to exist. They also are more common in women than in men. Rarely, they can be associated with the Birt–Hogg–Dubé syndrome, acromegaly, and polycystic ovary syndrome.

Skin tags may serve as a marker for those people whose carbohydrate metabolism is impaired and for those who may be at risk for diabetes mellitus type 2, although such a link has not been shown. Elevated blood sugar and insulin increase the incidence of skin tags through an unknown mechanism.