To determine if a genetic antioxidant strategy via overexpression of SOD1 is effective in rescuing CHD in a Notch1+/– background, we bred SOD1-overexpressing transgenic male mice (SOD1+) to diabetic Notch1+/– females to generate WT, Notch1+/–, SOD1+, and SOD1+ Notch1+/– compound-mutation embryos (n = 11 litters) (Figure 5A). The gene discussed is SOD1; the disease is coronary artery disorder.