Indeed, KRAS/TP53 co-mutated tumours promote TNF-driven pro-tumour inflammation [87], and increases in NK-specific MHC complexes (MICA/B) [87, 88], while KRAS/MYC co-mutation in lung cancer drives the recruitment of anti-inflammatory macrophages and the blocking of NK infiltration by CCL9 and IL-23 (Fig. 1, Fig. 2) [34]. This evidence concerns the gene KRAS and lung carcinoma.