The cell-autonomous mechanisms of KRAS indicate that its mutational activation can affect many tumor cellular processes within the tumor cells themselves, such as cell cycle, apoptosis, cell junctions, growth, self-renewal, and metabolic reprogramming.27–29 An association between KRAS and TAMs in cancers has been established by pioneering investigations.30,31 In agreement with these previous studies, our findings demonstrate that KRAS can induce functional reprogramming of TAMs in the context of CRC. This evidence concerns the gene KRAS and neoplasm.