In fact, the CDKN2A–CDKN2B locus is either bi- or monoallelicly deleted in 64% of BCR–ABL1-positive ALL cases and in 32–72% of T- or B-ALL cases without the BCR-ABL1 translocation, suggesting positive selection for cells with defective p16INK4A, p14ARF and p15INK4B (or some combinations thereof) during leukaemogenesis. Here, CDKN2A is linked to acute lymphoblastic leukemia.