We compared the B-ALL and AML patient-matched samples (designated 148752 and 152985, respectively), and while 46 oncoprotein-binding sites were detectable in the B-ALL sample at diagnosis, treatment with the menin inhibitor reduced the genome-wide MLL N and C terminal signal to undetectable levels (Fig. 7a, Supplementary Fig. 6a, b, Supplementary Data 2). This evidence concerns the gene KMT2A and acute myeloid leukemia.