Despite this, evidences exist about the existence of a genetic background that might involve the whole hematopoiesis and favor the development of BCP-ALL, e.g. in subjects with Down syndrome (DS) and a 30 fold increased risk for BCP-ALL [4], in individuals with germline mutations of the RUNX1, PAX5, ETV6, GATA1, HOXA11, ANKRD26, MPL, TP53 and RMB8A genes [5–8] and in children with RUNX1 amplification associated to t(15;21)(q10;q10) and a 3 × 103 fold increase in the frequency of BCP-ALL [9]. This evidence concerns the gene RUNX1 and Dravet syndrome.