Our mouse studies showed that abnormal myelopoiesis after IL-1rn deletion is mediated mainly through transcriptional activation of IL-1β-induced myeloid differentiation pathways at least partially dependent on NFκB activation in HSPC, which partially overlap with the transcriptional programs activated by long-term administration of high IL-1β doses as shown by reanalysis of publicly available datasets3,4 and are consistent with our findings in AML patients. The gene discussed is IL1B; the disease is acute myeloid leukemia.