Importantly, inactivation of the senescence program through loss of p53 is crucial also for tumor maintenance, as reinstating wild-type p53 in p53-null hepatocellular carcinomas in vivo triggers senescence associated with upregulation of inflammatory chemokines and cytokines that drive an innate immune response leading to tumor clearance involving enhanced NKG2D-dependent tumor elimination by natural killer cells [80,81]. This evidence concerns the gene KLRK1 and neoplasm.