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. The gene discussed is SMAD3; the disease is pemphigus foliaceus.