Other cells that have also been proposed as the origin of CAFs are adipocytes (48, 49), smooth muscle cells (44), and pericytes (50), which in response to TME molecules, such as TGF-β (48), platelet-derived growth factor (PDGF) (51), and connective tissue growth factor (CTGF) (52) acquire a CAF-like phenotype through cellular transdifferentiation, and consequently, participate in the promotion of carcinogenesis and tumor development (Figure 1). The gene discussed is TGFB1; the disease is neoplasm.