RB1 and neoplasm: In addition to stimulating cell cycle initiation via D-cyclin dependent kinases and Rb phosphorylation, these signaling pathways promote cell growth via mTOR activation and S6 phosphorylation, and it has been shown that inhibition of phosphorylation of both Rb and S6 is required for robust anti-tumor efficacy of drugs that inhibit cell signaling [6–12].