Inflammatory genes CXCL3 and CXCL8, as well as KMT2A (which interacts with Menin, a target of NPM1-mutated AML clinical trials [78]), have a high combined disruption score, as they are upregulated in immature AML cells compared to normal, with substantial differences in scale (Additional file 1: Fig. S8a, c). This evidence concerns the gene CXCL8 and acute myeloid leukemia.