Usually, a common form of treatment for the condition is a type of hand cream which moisturises the hard skin. However, currently the condition is incurable.

Beare–Stevenson cutis gyrata syndrome is so rare that a reliable incidence cannot be established as of yet; fewer than 20 patients with the condition have been reported.

Hermansky–Pudlak syndrome patients, families, and caregivers are encouraged to join the NIH Rare Lung Diseases Consortium Contact Registry. This is a privacy protected site that provides up-to-date information for individuals interested in the latest scientific news, trials, and treatments related to rare lung diseases.

While there is no cure for HPS, treatment for chronic hemorrhages associated with the disorder includes therapy with vitamin E and the antidiuretic dDAVP.

Management of AOS is largely symptomatic and aimed at treating the various congenital anomalies present in the individual. When the scalp and/or cranial bone defects are severe, early surgical intervention with grafting is indicated.

There is currently no specific treatment available for either of these so-called progeroid syndromes. With this in mind, what is most important when making a differential diagnosis with them is based on the prognosis, which appears to be far better in acrogeria.

Griscelli syndrome type 2 (also known as "partial albinism with immunodeficiency") is a rare autosomal recessive syndrome characterized by variable pigmentary dilution, hair with silvery metallic sheen, frequent pyogenic infections, neutropenia, and thrombocytopenia.

The overall prognosis is excellent in most cases. Most children with Adams–Oliver syndrome can likely expect to have a normal life span. However, individuals with more severe scalp and cranial defects may experience complications such as hemorrhage and meningitis, leading to long-term disability.

Acrogeria is extremely rare, with only about 40 cases having been reported in the medical literature, since 1941.

There is no known curative treatment presently. Hearing aids and cataract surgery may be of use. Control of seizures, heart failure and treatment of infection is important. Tube feeding may be needed.

Urbach–Wiethe disease is typically not a life-threatening condition. The life expectancy of these patients is normal as long as the potential side effects of thickening mucosa, such as respiratory obstruction, are properly addressed. Although this may require a tracheostomy or carbon dioxide laser surgery, such steps can help ensure that individuals with Urbach–Wiethe disease are able to live a full life. Oral dimethyl sulfoxide (DMSO) has been shown to reduce skin lesions, helping to minimize discomfort for these individuals.

Currently, there is no cure for Urbach–Wiethe disease although there are some ways to individually treat many of its symptoms. There has been some success with oral dimethyl sulfoxide (DMSO) and intralesional heparin, but this is not true in all cases. D-penicillamine has also shown promise, but has yet to have been used extensively. There are also some reports of patients being treated with etretinate, a drug typically prescribed to treat psoriasis. In some cases, calcifications in the brain can lead to abnormal electrical activity among neurons. Some patients are given anti-seizure medication to help deal with these abnormalities. Tracheostomy is often used to relieve upper respiratory tract infections. Carbon dioxide laser surgery of thickened vocal cords and beaded eyelid papules have improved these symptoms for patients. The discovery of the mutations of the ECM1 gene has opened the possibility of gene therapy or a recombinant EMC1 protein for Urbach–Wiethe disease treatment, but neither of these two options are currently available.

Oculocutaneous Albinism Type I or –Type 1A (OCA1A) is an autosomal recessive skin disease associated with albinism. This type of albinism is caused when the gene OCA1 does not function properly.

The location of OCA1 may be written as "11q1.4-q2.1", meaning it is on chromosome 11, long arm, somewhere in the range of band 1, sub-band 4, and band 2, sub-band 1.

Membranous aplasia cutis is a cutaneous condition, a type of aplasia cutis congenita, which can be seen along the embryonic fusion lines of the face.

There is no cure for Menkes disease. Early treatment with injections of copper supplements (in the form of acetate salts) may be of some slight benefit. Among 12 newborns who were diagnosed with MNK, 92% were alive at age 4.6. Other treatment is symptomatic and supportive. Treatments to help relieve some of the symptoms includes, pain medication, anti-seizure medication, feeding tube when necessary, and physical and occupational therapy.

A 2009 study reported results from 36 children who had received a stem cell transplant. At the time of follow-up (median time 62 months), 75% of the children were still alive.

As with all types of ichthyosis, there is no cure but the symptoms can be relieved.

- Moisturizers

- Prevention of overheating

- Eye drops (to prevent the eyes from becoming dried out)

- Systemic Retinoids (isotretinoin and acitretin are very effective, but careful monitoring for toxicity is required. Only severe cases may require intermittent therapy.)

Psychological therapy or support may be required as well.

Lenz–Majewski syndrome is a skin condition characterized by hyperostosis, craniodiaphyseal dysplasia, dwarfism, cutis laxa, proximal symphalangism, syndactyly, brachydactyly, mental retardation, enamel hypoplasia, and hypertelorism.

In 2013, whole-exome sequencing showed that a missense mutation resulting in overactive phosphatidylserine synthase 1 was the cause of LMS, making it the first known human disease to be caused by disrupted phosphatidylserine metabolism. The researchers suggested a link between the condition and bone metabolism.

Haemochromatosis type 3 is a type of Iron overload disorder associated with deficiencies in transferrin receptor 2. It exhibits an autosomal recessive inheritance pattern.

Several mutations in the FGFR2 gene (a gene coding for a protein called fibroblast growth factor receptor 2, which is involved in important signaling pathways) are known to cause Beare–Stevenson cutis gyrata syndrome; however, not all patients with the condition have a mutation in their FGFR2 gene. Any alternative underlying causes are currently unidentified. The syndrome follows an autosomal dominant pattern, meaning that if one of the two available genes carries a mutation the syndrome will result. Currently, no familial histories are known (in other words, there are no reports of cases in which a parent carrying a mutation in their FGFR2 gene then propagated said mutation to his or her child).

Cutis laxa (also known as chalazoderma, dermatochalasia, dermatolysis, dermatomegaly, generalized elastolysis, generalized elastorrhexis, or pachydermatocele) is a group of rare connective tissue disorders in which the skin becomes inelastic and hangs loosely in folds.

Many features of gerodermia osteodysplastica (GO) and another autosomal recessive form of cutis laxa, wrinkly skin syndrome (WSS, ""), are similar to such an extent that both disorders were believed to be variable phenotypes of a single disorder.

Several delineating factors, however, suggest that gerodermia osteodysplastica and wrinkly skin syndrome are distinct entities, but share the same clinic spectrum.

While the prevailing feature of wrinkly, loose skin is more localized with GO, it is usually systemic, yet eases in severity with age during the course of WSS. Also, as the fontanelles ("soft spots") are usually normal on the heads of infants with GO, they are often enlarged in WSS infants.

While WSS is associated with mutations of genes on chromosomes 2, 5, 7, 11 and 14; GO has been linked to mutations in the protein GORAB. A serum sialotransferrin type 2 pattern, also observed with WSS, is not present in GO patients.

But perhaps the most notable feature, differentiating GO from WSS and similar cutis laxa disorders, is the age-specific metaphyseal peg sometimes found in GO-affected long bone, near the knee. Not appearing until around age 4–5, then disappearing by physeal closure, this oddity of bone is thought to represent a specific genetic marker unique to GO and its effects on bone development.

One European study reported a rate of 1 in 254,000; a Japanese study reported a rate of 1 in 357,143. No correlation with other inherited characteristics, or with ethnic origin, is known.

Palmoplantar keratodermas are a heterogeneous group of disorders characterized by abnormal thickening of the palms and soles.

Autosomal recessive and dominant, X-linked, and acquired forms have all been described.

This includes Chediak-Higashi syndrome and Elejalde syndrome (neuroectodermal melanolysosomal disease).