The potential crosstalk between C-MYC and RB, which was demonstrated by simultaneous observation of RB loss and C-MYC overexpression in previous studies, [43,44] could explain how CDK2 inhibition may work even in the absence of RB, i.e., targeting CDK2 and CDK4/6 simultaneously can synergize to kill cancer cells via suppressing C-MYC and inducing senescence, independently of the RB status. The gene discussed is CDK2; the disease is cancer.