Thus, additional proliferative and survival advantages may be provided to MET amplified tumor cells by concomitant disruption of the p53 tumor-suppressive function, which relies on p53-mediated cell-cycle arrest or apoptosis in response to not only DNA damage and hypoxia, but also mitogenic oncogenes (such as mutant EGFR or amplified MET) [78,79,80,81]. The gene discussed is MET; the disease is neoplasm.