We therefore sequenced 41 selected genes that were either tyrosine kinases, within the PI3K/RAS pathways, epigenetic regulators, or recurrently mutated in KMT2A-R leukemia (see Methods and Supplementary Table 1) at a mean coverage of 3231 ± 1277 (s.d.)(Supplementary Data 1), in 62 primary (27 dominant and 7 subclonal KMT2A-MLLT3 and an activating mutation, and 28 KMT2A-MLLT3 alone) and 29 paired secondary recipients (derived from 15 dominant and 6 subclonal KMT2A-MLLT3 and an activating mutation, and 8 KMT2A-MLLT3 alone) (Supplementary Table 2). The gene discussed is MLLT3; the disease is leukemia.