These data show that in the absence of IL-6, miR-146a KO mice display a partially reduced HSC defect and less myeloproliferative disease, indicating that upregulation of the NF-κB-responsive proinflammatory cytokine IL-6 is an important driver of the HSC defect and myeloproliferative disease in miR-146a KO mice under chronic inflammatory stress induced by aging or repeated bacterial stimulation. The gene discussed is IL6; the disease is myeloproliferative disorder.