Major tumor suppressors pathways, such as these relying on pRB and/or protein 53 (p53), promote proapoptotic signals that ultimately converge on Mitochondrial Outer Membrane Permeabilization (MOMP).1 As a consequence, their loss in cancer cells results in failure to undergo MOMP in response to therapy, and approaches allowing to mitigate such defects are being actively investigated. This evidence concerns the gene TP53 and neoplasm.