The primary pathophysiological mechanism of PF involves the activation of both lung epithelial cells through epithelial-to-mesenchymal transition (EMT) and lung fibroblasts via fibroblast-to-myofibroblast transition (FMT), a process in which the profibrotic cytokine transforming growth factor β1 (TGFβ1) plays a pivotal role. This evidence concerns the gene TGFB1 and pemphigus foliaceus.