In TNBCs, RB1 is frequently disrupted by mutations/deletion/silencing, whereas in luminal and most HER2+ BC, pRB is often inactivated by hyper-phosphorylation, rendering these tumors responsive to CDK4/6 inhibitors such as palbociclib, abemaciclib and ribociclib, which induce dephosphorylation and activation of pRB [26, 27]. This evidence concerns the gene ERBB2 and breast cancer.