Severely injured burn patients receive multiple blood transfusions for anemia of critical illness despite the adverse consequences. One limiting factor to consider alternate treatment strategies is the lack of a reliable test platform to study molecular mechanisms of impaired erythropoiesis. This study illustrates how conditions resulting in high catecholamine microenvironment such as burns can instigate myelo-erythroid reprioritization influenced by beta-adrenergic stimulation leading to anemia. In mouse model of scald burn injury we observed, along with a 3-fold increase in bone marrow LSKs (lin^neg Sca1⁺cKit⁺), the myeloid shift is accompanied with a significant reduction in megakaryocyte erythrocyte progenitors (MEPs). Beta-blocker administration (propranolol) for six days post burn not only reduced the number of LSKs and MafB⁺ cells in multi potent progenitors but also influenced myelo-erythroid bifurcation by increasing the MEPs and reducing the granulocyte monocyte progenitors (GMPs) in the bone marrow of burn mice. Furthermore, similar results were observed in burn patients' PBMC derived ex-vivo culture system demonstrating that commitment stage of erythropoiesis is impaired in burn patients and intervention with propranolol (non-selective beta 1,2-adrenergic blocker) increases MEPs. Also, MafB⁺ cells that were significantly increased following standard burn care could be mitigated when propranolol was administered to burn patients establishing the mechanistic regulation of erythroid commitment by myeloid regulatory transcription factor MafB. Overall, results demonstrate that beta- adrenergic blockers following burn injury can redirect the hematopoietic commitment toward erythroid lineage by lowering MafB expression in multi potent progenitors and be of potential therapeutic value to increase erythropoietin responsiveness in burn patients.