However, an intrinsic defect in neurons of increased susceptibility to ischemia in embryonic EpoR−/− mice was observed in neurons from embryonic mice with selective EpoR expression driven by the endogenous EpoR promoter in hematopoietic/endothelial tissue but not in brain, which rescues the severe anemia associated with EpoR−/− mice [111]. This evidence concerns the gene EPOR and anemia.