On the other hand, loss-of-function mutations in human VDR results in disrupted VDR-DNA binding or VDR-RXR heterodimerization; this impaired corepressor activity on VDR-mediated transactivation, in part due to the attenuated interaction of hairless with HDACs, can result in clinical conditions, such as the rare autosomal recessive disease atrichia with papular lesions or alopecia universalis congenita (42-44). The gene discussed is VDR; the disease is alopecia universalis congenita.