CDKN2A, also known as cyclin-dependent kinase Inhibitor 2A, is ubiquitously expressed in many tissues and cell types. p19ARF activates the p53 tumor suppressor. Somatic mutations of CDKN2A are common in the majority of human cancers, with estimates that CDKN2A is the second most commonly inactivated gene in cancer after p53. p19ARF, which is unrelated to p16, arises from transcription of an alternative reading frame of the p16 gene. Like p16, p19ARF has been shown to induce cell cycle arrest. Mice lacking p19 ARF but expressing functional p16 have been shown to develop tumors early in life.
