A recent observation that an increase in Dsg 1 antibody titer in a PV patient has occurred already after the patient had started treatment and went into clinical remission [120] supports the notion that anti-Dsg antibodies “witness” rather than trigger PV, i.e. that production of these autoantibodies is the result rather than the cause of epidermal blistering in pemphigus [121]. The gene discussed is DSG1; the disease is pemphigus.