Several studies suggest the potential involvement of the JAK-STAT functional pathway in human pemphigus via the following mechanisms: (i) overexpression of JAK-signaling cytokines (e.g., IL-6 and IL-21) important for autoantibody production in pemphigus, and (ii) JAK1/JAK3 inhibitors demonstrate a protective effect on keratinocyte cell acantholysis after incubation with pemphigus autoantibodies, suggesting a potential involvement of JAK/STAT molecules during blister formation in pemphigus disease [3]. Here, SOAT1 is linked to pemphigus.