Furthermore, KMT2A-MLLT3-driven infant ALL (IC4) exhibited a distinct profile of cooperating genetic alterations with frequent CNAs and mutations in PAX5 and cell cycle regulators (CDKN2A/B and CCND3), indicating a unique pathogenesis of this subgroup among KMT2A-r infant ALL. Here, MLLT3 is linked to acute lymphoblastic leukemia.