Over the years numerous genetic abnormalities in T-ALL have been identified, including chromosomal rearrangements involving T-cell receptor (TCR) loci, activating mutations of NOTCH1, 9p21.3 deletions associated with impairment of CDKN2A/2B cell-cycle regulators and ectopic expression of several transcription factors, acting as oncogenes, including: TAL1, LYL1, TLX1/3, HOXA9/10, NKX2-1 and LMO1/2 [3]. The gene discussed is CDKN2A; the disease is acute lymphoblastic leukemia.