And Zhou et al. suggested that γδ T cells, instead of Th17 cells, were the primary source of IL-17 in infarcted heart, and the increase of IL-17 significantly expanded infarct size, worsened cardiac function, aggravated myocardial fibrosis and cardiomyocyte apoptosis in post-AMI patients. Here, IL17A is linked to Myocardial fibrosis.