It has been hypothesized, however, that an infectious agent can precipitate development of B-ALL in a genetically susceptible individual.14, -16 The most common translocation occurring in pediatric B-ALL is ETV6-RUNX1 [t(12;21)].15,16 In this context, Greaves proposed a 2-hit model for childhood acute leukemia. Here, RUNX1 is linked to precursor B-cell acute lymphoblastic leukemia.