The association may be explained by multiple mechanisms: (1) iron sequestration and macrophage iron overload promoted by hepcidin, leading to oxidative stress and vascular damage; (2) pro-inflammatory effects, as suggested by correlations with CRP; and (3) an indirect link with anemia management, since patients in higher tertiles were more frequently treated with intravenous iron and ESA therapy. The gene discussed is CRP; the disease is anemia.