Previous studies have highlighted the role of TGF‐β1‐SMAD3 activation in FMT and subsequent PF progression.[30] SNX9 has been demonstrated to promote SMAD3 phosphorylation and nuclear translocation.[31] Therefore, we hypothesized that endocytic rCTSK facilitated SMAD3 activation through SNX9 for COL1A1 production. The gene discussed is COL1A1; the disease is pemphigus foliaceus.