[citation needed] Mutations in the EDA, EDAR, and EDARADD genes cause hypohidrotic ectodermal dysplasia.

The EDA, EDAR, and EDARADD genes provide instructions for making proteins that work together during embryonic development.

Ectoderm-mesoderm interactions are essential for the formation of several structures that arise from the ectoderm, including the skin, hair, nails, teeth, and sweat glands.

[citation needed] In X-linked recessive inheritance, a female with one altered copy of the gene in each cell is called a carrier.

These signs and symptoms are usually mild and include a few missing or abnormal teeth, sparse hair, and some problems with sweat gland function.

In January 2013, Edimer Pharmaceuticals, a biotechnology company based in Cambridge, MA, USA, initiated a Phase I, open-label, safety and pharmacokinetic clinical study of EDI200, a drug aimed at the treatment of XLHED.

During development in mice and dogs EDI200 has been shown to substitute for the altered or missing protein resulting from the EDA mutation which causes XLHED.

[3] As the treated group "didn’t see significant changes in sweat gland function and other early markers of biologic activity",[4] prenatal administration of the drug was considered.