In one preclinical model of sepsis, HMGB1 induced anemia, led to reduced expansion, especially at the CFU stage, increased the death of EPO-sensitive erythroid precursors in human models of erythropoiesis, and significantly attenuated EPO-mediated phosphorylation of the Janus kinase 2/STAT5 and mTOR signaling pathways. This evidence concerns the gene EPO and Sepsis.