Renal fibrosis is a major contributor to the development of CKD, and given the significance of EPOR/βcR heterodimer in EPO-conferred nonhematopoietic protection, in the present study, we aimed to investigate how the process of tubulointersticial fibrosis can be influenced by the coexpression of the EPOR/βcR heterodimer and the administration of rEPO in Ad-CKD model. The gene discussed is EPOR; the disease is chronic kidney disease.