Analysis of clinical samples has demonstrated that KRAS mutations are associated with an immunosuppressive tumor microenvironment (TME; ref. 13), and preclinical studies have identified a number of mechanisms by which oncogenic KRAS can drive immune evasion including promoting the expression of numerous immunosuppressive myeloid chemoattractants (14, 15) and immune checkpoint ligands (16). Here, KRAS is linked to neoplasm.