TAMs in PDAC can be divided into an antitumor M1 phenotype (activated by lipopolysaccharide, TNF-α and IFN-γ, expressing higher levels of IL-12, IL-23, MHC II, and inducible nitric oxide synthase) and a tumor-promoting M2 phenotype (activated by IL-4 and IL-13, expressing higher levels of IL-10 and TGF-β) [71]. This evidence concerns the gene TGFB1 and neoplasm.