Intriguingly, G2/M exit from the cell cycle distinguishes DIPS ovarian cancer cells from their counterparts undergoing replicative senescence, in which senescence-associated growth arrest occurred in the G1 phase and involved elevated cyclin D1, whose level in DIPS cells [29] and other cellular models undergoing G2/M phase block [30] was unchanged. Here, CCND1 is linked to ovarian cancer.