This concept could be applied to 1) inhibit other factors disrupting MDM2-mutp53 interaction, such as HSP90 and BAG2 (Li et al., 2011b; Yue et al., 2015); or 2) tip the dynamics of MDM2-mutp53 interaction towards p53 degradation to amplify MDM2’s anti-tumorigenic functions in cancers possessing mutp53 (Yang et al., 2019). Here, TP53 is linked to cancer.