This therapeutic strategy involves augmenting the inherent synthesis of erythrocytes, ensuring ample iron levels for hemoglobin formation, reducing cytokine production and release, implementing antioxidative and anti-inflammatory processes, suppressing hepcidin, and addressing anemia (49), overseeing and safeguarding renal EPO-producing cells (REPs) during stressful conditions for the treatment of renal anemia (50, 51), enhancing the production of endogenous EPO, optimizing iron utilization under hypoxia (52), inhibiting prolyl hydroxylases, and modulating hepcidin activity (53). The gene discussed is HAMP; the disease is anemia (phenotype).