These genomic alterations not only change the hallmarks of cancer fundamental cellular pathways such as the p53/RB cell cycle pathway, the RTK/PI3K/mTOR proliferative pathway, and the histone modification chromatin regulatory network, which become potential druggable targets for UBC25, but they also produce many non-self, or “foreign” proteins, which could be recognized by activated effector T cells and potentiate cancer cells responding to immune checkpoint inhibitors26. The gene discussed is RB1; the disease is cancer.