This hypothesis is supported by the fact that haematopoietic progenitor cells (Ba/f3) expressing variant p16INK4A were substantially more susceptible to BCR–ABL1-mediated leukaemic transformation compared with cells with the wild-type protein (Fig. 2a), pointing to rs3731249 as a possible functional variant directly contributing to the association with ALL risk. This evidence concerns the gene CDKN2A and acute lymphoblastic leukemia.