,7,8,9 Consequently, pharmacologically targeting the de-stabilization/disruption of C-terminal RING domain dimerization is considered an attractive and underexploited approach to inhibiting MDM2/MDMX, offering a potentially viable therapeutic strategy against MDM2/MDMX-dependent cancers, irrespective of TP53 mutational status.5 This evidence concerns the gene MDM4 and cancer.