Cancer cells with mutated p53 have accelerated tumor growth associated with increased VEGF expression and neovascularization34,35, which serves an important survival pathway, resulting in a therapeutic advantage of VEGF-inhibition in patients with p53 mutant malignancies, which was supported by our finding that VEGF inhibition-based therapies led to significantly longer PFS in patients with a mutated TP53 than in patients with wild-type TP5336–39. The gene discussed is TP53; the disease is cancer.