Within the past two decades, similar mechanisms of cell cycle arrest, potentially resulting in growth deceleration and senescence, have been described in several cancers driven by activation of the RAS–RAF–mitogen-activated protein kinase (MAPK) pathway, MYC activation, hyperactivated WNT-β-catenin signaling, activation of the INK4A-RB pathway, or loss of PTEN [93,94,95,96,97,98,99]. Here, CDKN2A is linked to cancer.