Histological analysis of Senp1−/−;Ripk1D138N/D138N fetal lives showed a disproportionate abundance of immature erythroblasts as seen in Senp1−/− fetal livers, compared with that of WT fetal livers (Fig. 3g), suggesting that erythropoiesis defects leading to anemia in Senp1−/− embryos was not rescued by RIPK1-D138N mutation. The gene discussed is SENP1; the disease is anemia.