With this metabolic shift, KRAS-driven tumors not only are able to produce key lipid mediators establishing an immunosuppressive tumor microenvironment (TME), but are also able to take full advantage of exogenous lipids produced by the TME such as fatty acids (FAs) prostaglandins and other lipid mediators, thus maintaining a vicious cycle that allows tumor growth and metastasis. This evidence concerns the gene KRAS and neoplasm.