With the use of CRISPR-Cas9 genome editing, small-molecule inhibition and RNA-seq, the authors proved that KMT2A and DOT1L control the expression of HOX, MEIS1 and FLT3 (which is a downstream target of MEIS1), and also cell differentiation in NPM1-mutated leukemia, despite the lack of KMT2A rearrangement [139]. The gene discussed is KMT2A; the disease is leukemia.