We found no evidence for increased abundance of CBFB exons 1–5 in CBFB::MYH11 AMLs, relative to RUNX1::RUNX1T1 or NPM1c-mutated AMLs (Figure 8E), suggesting that the transcriptional activity of the CBFB locus is not substantially altered by the fusion in primary AML cells. The gene discussed is RUNX1T1; the disease is acute myeloid leukemia.