It is commonly acknowledged that the TGF-β/Smad signaling pathway serves an essential function in tumor fibrosis.25 The inactivation of the TGF-β/Smad signaling pathway in CAFs can lead to the suppression of CAF activation and pro-fibrotic factor secretion, the inhibition of CAF-mediated ECM remodeling, the downregulation of CAF-induced tumor cell invasion and metastasis, and the reversal of the pro-tumorigenic effects exerted by CAFs on therapy resistance. This evidence concerns the gene TGFB1 and neoplasm.