Indeed, the BCP-ALL with distinct MEF2D fusions also relies on hyperactivation of the pre-BCR signaling pathway to evade apoptosis and maintain the leukemogenic ability.10 Previously, our group identified a signature gene set related to MH (+) patients, which could be used for disease stratification even beyond MEF2D fusion BCP-ALL.33 In both MH and MB fusion cell systems, histone H3 acetylation activated the PI3K/AKT signaling pathway while multiple genes involved in this cascade were located in SEs (Fig. 3a–d). This evidence concerns the gene BCR and acute lymphoblastic leukemia.