The concurrent development of EBA mediated by a Th1/Th17-driven cutaneous autoimmune disease and immune-mediated thrombocytopenia in our patient raises the possibility that DPP-4 inhibition can precipitate a “multi-organ autoimmunity syndrome.” This concept is supported by reports describing DPP-4 inhibition–associated thyroiditis, arthritis, and other immune-mediated conditions, suggesting that the loss of CD26-dependent regulatory control may lower the threshold for autoimmune activation in genetically or immunologically susceptible hosts. The gene discussed is DPP4; the disease is acquired epidermolysis bullosa.