In human diploid fibroblasts, JMJD3 serves as a tumor suppressor by binding to and activating the INK4A-ARF locus [7, 8], while in T cell acute lymphoblastic leukemia, it functions as an oncogene required for leukemia initiation and maintenance [9, 10]. This evidence concerns the gene CDKN2A and T-cell acute lymphoblastic leukemia.