The lack of a functional G1/S cell cycle checkpoint in TP53-deficient tumors tends to be overdependence on the G2/M checkpoint, in which case inhibition of key regulatory proteins in the G2/M checkpoint, such as WEE1, directs tumor cells into apoptosis or increases sensitivity to other therapeutic approaches by blocking the cell cycle [93–95]. The gene discussed is TP53; the disease is neoplasm.