It has also been observed that tumor cells that survive HER2-blockade retain a high expression of cyclin D1 and, when targeted with CDK 4/6 inhibitors, become re-sensitized to anti-HER2 therapy by not only reducing the retinoblastoma phosphorylation, but also by suppressing mTORC1/S6K/S6RP activity and increasing tumor cell dependence on epidermal growth factor receptor family kinases14–16. Here, EGFR is linked to neoplasm.