AML mutations, even those that do not directly control gene expression, co-opt the transcriptional and epigenetic machinery to alter chromatin states, 3D DNA topology, and communication between enhancers and promoters to generate leukemia-specific transcriptional programs; hallmark change is the activation of expression of inflammatory cytokine genes via the transcription factor NFκB [61]. The gene discussed is NFKB1; the disease is leukemia.