Aberrant activation and proliferation of myofibroblasts appear to be positively related to the pathogenesis of PF (Figure 6) [135,136], which can synthesize pro-fibrotic proteins including α-smooth muscle actin (α-SMA), collagen I and III, and fibronectin, finally resulting in excessive secretion and accumulation of ECM [137,138]. The gene discussed is ACTA1; the disease is pemphigus foliaceus.