In previous experiments, MEF2D fusions, especially MH and MB, have been shown to impede B cell development at the pre-B stage, upregulate the expression of genes involved in pre-BCR signaling, and provide survival advantage in MEF2D fusion-containing BCP-ALL cell lines.6,10,11 In a murine MH knock-in model, an early-stage B-cell development blockade has been noticed, which, in collaboration with NRAS mutation (MH/NRASG12D), could develop towards a full-blown BCP-ALL. The gene discussed is BCR; the disease is acute lymphoblastic leukemia.