SGLT2i improve erythropoietin expression/secretion via at least three distinct mechanisms: modulation of tubulointerstitial hypoxia and hypoxia-induced factor (HIF)‐α expression, mitigation of inflammation-induced functional iron deficiency, and metabolic reprogramming (the latter manifested at a cellular level by an increased production of ketone bodies and a state of starvation mimicry) [104]. The gene discussed is EPO; the disease is Iron deficiency anemia.