This mechanism is important since the standard hypothesis describing PF pathogenesis is based on the activation of various populations of macrophages and lymphocytes, resulting in cytokines and chemokines production enhancement which leads to the activation of fibroblasts and myofibroblasts and the subsequent induction of transforming growth factor beta 1 (TGFβ1) and accumulation of abnormal extracellular matrix [50]. Here, TGFB1 is linked to pemphigus foliaceus.