Furthermore, the role of anti-AChR antibodies in pemphigus pathogenesis is supported by observations of intraepidermal splits and acantholysis in pemphigus vulgaris patients lacking anti-Dsg1/3 antibodies, as well as by disruptions in normal keratinocyte morphology following prolonged exposure to anti-AChR autoantibodies [6,7]. The gene discussed is DSG1; the disease is pemphigus.