CDKN2A and leukemia: If not prevented by an epigenetic influence, the AP-1 family of proteins can also block cell cycle and promote senescence and apoptosis through transcriptional up-regulation of both DAPK1 and RUNX3, as well as p16INK4A/CDKN2A.[4, 7, 21, 22] Epigenetically repressed p16INK4A/CDKN2A promotes leukemia stem cell upregulation,[23] which is observed in normal karyotype Flt3ITD+ve and complex karyotype AMLs.[23] However, p16INK4A/CDKN2A repression is not observed in good-risk [eg. core-binding factor-associated (CBF+ve)] AMLs.[23-25]