The Dsg compensation hypothesis maintains that anti-Dsg 1 and 3 antibody profiles in pemphigus sera and the normal epidermal distributions of Dsg 1 and 3 determine the sites of blister formation and that either Dsg 1 or Dsg 3 alone is sufficient to maintain keratinocyte adhesion [42]. The gene discussed is DSG1; the disease is pemphigus.