In conclusion, by the use of an in vitro model further corroborated on BM patient-derived CD34+ HSPCs, we show for the first time that hyperglycemia induces marked epigenetic changes responsible for long-term proinflammatory priming of HSPCs, which, once transmitted to the cell progeny, contribute to persistent and pathogenic changes in immune cell function and composition even after the original stimulus (HG) was removed. The gene discussed is CD34; the disease is Hyperglycemia.