In addition, we proved that downregulation of tRF-5014a in HG-treated cardiomyocytes significantly abolished the decrease in cell viability and increase in cell death as well as IL-1β and IL-18 levels, suggesting that tRF-5014a might play a critical role in cardiomyocyte injury associated with DCM. This evidence concerns the gene IL1B and familial dilated cardiomyopathy.