Despite the small number of patients, which makes the accurate assessment of additional genetic associations more difficult, concurrent genetic aberrations occurred more frequently in epigenetic modifiers, with a trend towards BCORL1, EZH2, and KDM6A. A propensity for association was noted for spliceosome U2AF1, whereas other spliceosome-related genetic aberrations were absent in RUNX1-mutated paediatric AML. This evidence concerns the gene KDM6A and acute myeloid leukemia.