has shown using different genetic and protein degradation techniques in vitro and genetically in vivo to demonstrate AML cells’ reliance on IRF2BP2, which is shown to suppress IL-1β/TNFα signaling via NF-κB, and IRF2BP2 disruption causes an acute inflammatory state that culminates in AML cell death (130). The gene discussed is IL1B; the disease is acute myeloid leukemia.