The impaired EPO responsivenessin CKD rats could be attributed to excess proinflammatory cytokines.51 These cytokines may directly downregulate EPORexpression or indirectly inhibit the growth of erythroid progenitorcells that express EPOR at very high levels52 and consequently leads to the decline of downstream ERFE responses.These findings suggest the potential of ERFE as a biomarker for predictingrHuEPO efficacy, as reduced precursor cell mass or impaired rHuEPOresponsiveness is expected to lead to compromised erythroid response. The gene discussed is EPOR; the disease is chronic kidney disease.