The current body of knowledge in the pemphigus foliaceus (PF) field points to an evident multistep model of disease pathogenesis characterized by blister formation and acantholysis which most likely associated with downstream events following the binding of desmoglein-1- (Dsg1-) specific IgG pathogenic autoantibodies (-Abs) [1, 2]. Here, DSG1 is linked to pemphigus.