The 6β-OHT treatment restored the effect of Ang II to cause endothelial dysfunction in both the intact Cyp1b1−/− and castrated Cyp1b1+/+ and Cyp1b1−/− mice (59%, 50%, 53%, respectively) as determined by the loss of relaxation of the aorta by ACh (88%) (Fig. 2c, d). The gene discussed is AGT; the disease is endothelial dysfunction.