Introduction: The retinoblastoma tumor suppressor (RB) is an important regulator of the cell cycle and a multitude of other processes that are germane to tumor development. The functional inactivation of RB has been recognized to occur sporadically in a large fraction of human tumors where it is believed to contribute to disease initiation and/or progression. Several studies have now shown that the specific loss of this tumor suppressor represents a selective vulnerability that could be targeted therapeutically and therefore provide a precision approach to exploiting RB loss [1-5].