Since Sema3A is known to inhibit the intraepidermal extension of peripheral nerves and has been reported to abolish the growth-promoting effect of NGF on sensory afferents in the adult rat spinal cord and mouse embryonic neurons30–32, the epidermal innervation in AD and psoriasis is likely to be regulated by a balance of NGF and Sema3A, and the decreased Sema3A expression in the epidermis of these patients could result from increased NGF levels. The gene discussed is SEMA3A; the disease is Alzheimer disease.