As a signaling molecule for myocardial infarction and ROS activation, overexpression of heart-specific transgenic CaMKII has also been found to cause myocardial hypertrophy, heart failure, and premature death.127 In addition, it has been found that elevated circulatory TMAO levels increase the likelihood of developing heart failure, as they are associated with pathological dilatation of the left ventricle, reduced left ventricular ejection fraction, increased circulating BNP levels, and increased pulmonary edema and myocardial fibrosis128. This evidence concerns the gene CAMK2G and heart failure.