Based on the fact that most mutations, such as SMAD4 and KRAS, are a downstream signaling factor of TGFβR, and the fact that the mutations of TGFβR accounts for 4–7% of pancreatic cancers [90,91], it can be observed that the formation of PDAC TME is mostly driven by the paracrine or autocrine manner of TGF-β. This evidence concerns the gene KRAS and familial pancreatic carcinoma.