In this context, a subtype with MEF2D gene fused to multiple partners, accounting for about 5% of BCP-ALL, has drawn attention of hematology/oncology community.1,2 Characterized by clonal expansion of lymphoblasts at the pre-B cell stage, this subtype exhibits poor clinical prognosis, with 5-year OS rates of 33.3% in children and merely 15.6% in adults.4 Patients are generally unresponsive to conventional treatment regimens and HSCT.6 Therefore, there is an urgent need for effective therapeutic strategies against this BCP-ALL subtype. This evidence concerns the gene MEF2D and acute lymphoblastic leukemia.