In addition to promoting cancer cell survival and proliferation, KRAS mutants also favor the formation of a highly immunosuppressive tumor microenvironment (TME) through several mechanisms, including repressing interferon regulatory factors (IRFs) 7,8, increased secretion of immunosuppressive cytokines (i.e., TGF-β and IL-10) 9, activating the JAK-STAT3 signaling pathway 10, triggering the downregulation of MHC-I in tumor cells 11, and synergizing with other mutations, such as mutations in the TP53 gene 12. The gene discussed is TP53; the disease is neoplasm.