KRAS promotes Cyclin D1-dependent cell proliferation, suppresses apoptosis by promoting the expression of BCL-2 family proteins, rewires cancer metabolism covering glycolysis, glutaminolysis, macropinocytosis, mitophagy, redox balance, and macromolecule biosynthesis of amino acids, nucleotides and fatty acids (see review 9), remodels tumor microenvironment (TME) to facilitate tumor growth 10-13, and protects tumor cells from immune surveillance 10, 14-17. This evidence concerns the gene KRAS and cancer.