(ii) Cyclin-dependent kinase 4 (Cdk4) (G1 transition/cell cycle progressor) and its inhibitor proteins, p16INK4A, p15INK4B, p18INK4C and p19INK4D, cause KRAS mutated lung cells to undergo senescence and prevent tumor growth128 (iii) TANK-binding kinase 1 (TBK1), serine-threonine kinase STK33 and polo-like kinase 1(PLK1) are other potential synthetic lethal therapeutic targets that have been identified in cell lines [79–81]. The gene discussed is KRAS; the disease is neoplasm.