The pathogenesis resembles the one of bullous pemphigoid, with the presence of IgG autoantibodies against BP180 * and, in part, against BP230 *, constituents of the hemidesmosome, leading to the detachment of the dermis and epidermis and the emergence of blisters, inflammation and erosions [1]. The gene discussed is COL17A1; the disease is bullous pemphigoid.