Such a dual inhibitory strategy could be especially beneficial in the treatment of MYC-driven MB, given that elevated MYC levels have been shown to sensitize cancer cells to the inhibition of mitosis and checkpoint signaling by increasing apoptosis65,83, since CHEK1 signaling activation is correlated with cell survival and poor prognosis in MYC-driven MB84. The gene discussed is CHEK1; the disease is cancer.