The pathogenesis of pulmonary fibrosis (PF) has long been known to closely linked with the differentiation of pulmonary microvascular pericytes into myofibroblasts and abnormal deposition of extracellular matrix, which was mediated by the alterations of the TGF‐β1/Smad3/β‐catenin signalling cascade5, 6, 7; however, the regulatory mechanisms of this signalling axis during pericyte transformation and fibrosis remain poorly understood. This evidence concerns the gene TGFB1 and pemphigus foliaceus.