The direct regulation of GATA1 expression by TR2 and TR4 described above, would explain why transgenic mice overexpressing TR4 alone (TgTR4) or both TR4 and TR2 (TgTR2/TR4) present a transient midembryonic anemia and defects in primitive erythroid precursor formation, which could not be explained simply by the effects of the TR2/TR4 protein complex on globins gene transcription [114]. The gene discussed is NR2C1; the disease is anemia (phenotype).