While aberrant RAS/MAPK pathway signaling is attributed a critical role in oncogenesis, cancer cell survival, dissemination, and drug resistance in a variety of human cancers, in vitro studies have repeatedly shown an induction of cell cycle arrest in G1 due to the accumulation of cell cycle inhibitors p53 and p16INK4a and a decreased expression of cyclin A following persistent oncogenic RAS/MAPK signaling in murine and human cells [92,100,105,106,107,108,109,110,111]. The gene discussed is CCNA2; the disease is cancer.