Infant acute lymphoblastic leukemia (iALL) is an aggressive disease that remains a major clinical challenge.1, 2, 3 In 70% to 80% of iALL, translocations of KMT2A gene, most commonly with AFF1 [t(4;11) (q21;q23)], produce an oncogenic fusion protein which recruits a large protein complex, "rewriting" epigenetic marks to alter expression of target genes.4, 5, 6 Understanding the KMT2A fusion protein complex has been vital for identifying targets such as menin for novel therapies.7 This evidence concerns the gene AFF1 and acute lymphoblastic leukemia.