In this study, we utilized the exon-16 disrupted murine model of hemophilia A on predominantly a C57Bl/6 genetic background, which previously was shown to produce higher anti-fVIII inhibitory antibodies than the Balb/c model of hemophilia A.34 Using this model, two animals developed inhibitors to ET3, as evidenced by loss of fVIII activity and confirmed by ELISA and Bethesda assays. The gene discussed is EDN3; the disease is hemophilia A.