Given the existence of immunogenetic subtypes of BCP-ALL, it is perhaps not surprising there is variability in the genetic effects on ALL risk by subtype, with 10q21.2 variants influencing hyperdiploid ALL and 10p14 variants influencing non-hyperdiploid/non-ETV6-RUNX1 disease.6, 7 In contrast to the 7p12.2 and 10p12.2 risk variants,6, 7 the 10q26.13 and 12q23.1 loci have generic effects on the development of ALL. This evidence concerns the gene RUNX1 and acute lymphoblastic leukemia.