STAT5-deficient fetuses ultimately develop severe anemia and die in the perinatal period [29], but show no absolute block in definitive erythropoiesis or any known primitive erythroid defect, suggesting that other transcriptional regulators are also involved in mediating this critical signal and supporting our computational prediction of a differential role for STAT-signaling in primitive compared to definitive erythropoiesis. This evidence concerns the gene SOAT1 and anemia (phenotype).