Moderate activation reduces oxidative stress and inhibits apoptosis, but excessive activation promotes myocardial hypertrophy and fibrosis through the mTOR and NF-κB pathways, and STAT3-deficient mice have reduced myocardial capillaries and interstitial fibrosis, ultimately leading to dilated cardiomyopathy [35,36]. This evidence concerns the gene NFKB1 and dilated cardiomyopathy.