The pathophysiology relating anemia to HF in humans is multifactorial, including renal dysfunction and impaired erythropoietin production [5], overproduction of proinflammatory cytokines such as tumor necrosis factor and interleukins [14, 15], an expansion in plasma volume [16], and downregulation of erythropoietin, such as by angiotensin-converting enzyme inhibitors [17]. This evidence concerns the gene EPO and anemia.