Pharmacological disruption of IGF2BP1-RNA interactions with small molecules such as BT and CUB abolishes its binding to MDM2 and PD-L1 mRNAs, mirroring effects seen with E2F1-3 and MYCN.39,51 These inhibitors impair tumor cell viability while sparing T cells and restore antitumor immunity by enhancing CTL and T helper cell activation. Here, MDM2 is linked to neoplasm.