Recent studies in Kras-driven and p53-deficient lung adenocarcinomas demonstrated that treatment with a combination of inhibitors that target MEK1/2 of the mitogen-activated protein kinase pathway and cyclin-dependent kinase (CDK) 4 and CDK6 could induce an RB-dependent senescence program that would activate an NK-cell-dependent destruction of tumors cells25. Here, KRAS is linked to lung adenocarcinoma.