Several studies have shown increased levels of interleukin 10 (IL-10) and TGF-β in the serum and tumor tissue of KRAS-mutant pancreatic and lung cancer patients.232–236 Some authors also observed that mutations in KRAS increase the secretion of these two anti-inflammatory molecules in PDAC, NSCLC and CRC, which cause M2 macrophages recruitment to the tumor site.237,238 Moreover, in KRAS-mutant lung tumors, IL-6 inhibition reduces anti-inflammatory macrophages,215 suggesting that KRAS-induced IL-6 might also be responsible for the M2 macrophages recruitment. Here, TGFB1 is linked to neoplasm.