In the field of pemphigus research the so-called “desmoglein compensation hypothesis” was established to explain that some Dsg isoforms can compensate for each other: when autoantibodies are present in pemphigus patients targeting both Dsg1 and Dsg3, they may bind as an initial event to the extracellular domain of desmosomal cadherins, disrupt intercellular binding and lead to epidermal blister formation. The gene discussed is DSG3; the disease is pemphigus.