Moreover, IL-6 plays a central role in myocardial fibrosis that depends on the activation of the MAPK and STAT3 pathways (46), experiments have shown that this upregulation contributes to cardiac hypertrophy and early mortality in mice (47), suggesting that of IL-6/STAT3 signaling pathway may promote cardiac fibrosis and hypertrophy, and offer a new target for cardiomyopathy (48). This evidence concerns the gene STAT3 and cardiac hypertrophy.