We therefore consider the MYC-RUVBL1 axis to be a targetable vulnerability in cancer cells, since the RUVBL1/2 complex is a druggable AAA ATPase.56 In fact, the allosteric RUVBL1/2 inhibitor CB-6644 had previously been shown to arrest Ewing sarcoma and multiple myeloma in immunocompromised mice49 54 and had a striking therapeutic effect on pancreatic tumours at tolerated concentrations in immunocompetent mice in our study. Here, MYC is linked to cancer.