Inconsistent with the above findings, all the eight studies concluded that the autophagy status was inhibited during SI-AKI, while the renal protective effects exerting by specific interventions (i.e., temsirolimus, rapamycin, recombinant human erythropoietin, umbilical cord blood mononuclear cells, Procyanidin B2, dexmedetomidine, and NF-κB inhibitor 270) might be contributed by the elevation of autophagy. The gene discussed is EPO; the disease is acute kidney injury.