Cancer cells overcome the growth constraints that govern normal cells by inactivating cell cycle checkpoints (through the upregulation of aurora kinase A and polo-like kinase 1, PLK1), tolerating DNA damage (primarily through deletion/degradation of TP53) and abrogating senescence (through the inactivation of TP53 and inhibition of cyclin-dependent kinase inhibitor 1, CDKN1A, best known as p21) [136]. The gene discussed is PLK1; the disease is cancer.