In the kidney, resident fibroblasts produce erythropoietin (EPO) in response to hypoxic insults to maintain homeostasis under physiologic condition, whereas, under pathologic conditions, resident fibroblasts transdifferentiate into myofibroblasts, which execute renal fibrosis by producing large amounts of extracellular matrix proteins, at the cost of EPO production [1, 2]. This evidence concerns the gene EPO and renal fibrosis.