Since the D281G is a gain of function TP53 mutation causing disruption of a spindle checkpoint and promoting genetic instability23, it might be possible that disruption of DDR checkpoints due to ATM inhibition and of spindle checkpoints linked to the D281G mutation synergized and cooperated to inhibit the tumor growth in the Biddlestone-Thorpe study. The gene discussed is TP53; the disease is neoplasm.