SOD3-knockout mice had greater increases of nitrotyrosine in the peri-infarct myocardium, and this was associated with a greater reduction of LV ejection fraction, a greater decrease of sarcoplasmic or endoplasmic reticulum Calcium2+ ATPase, and a greater increase of atrial natriuretic peptide in the peri-infarct zone compared to wild-type mice at 8 weeks after MI, which means that mice with SOD3 gene deletion developed more severe LV hypertrophy, more fibrosis, and worse cardiac function [54]. The gene discussed is SOD3; the disease is myocardial infarction.