Furthermore, the essential role of loss of functional p53 in GTML/Trp53KI/KI tumor growth suggests additional opportunities for intervention with emerging therapeutics that reactivate wild-type P53 by inhibiting the P53-MDM2 interaction (Carol et al., 2013; Chène, 2003; Van Maerken et al., 2014). This evidence concerns the gene MDM2 and neoplasm.