Recent studies have shown that miR-21 is abundantly expressed in the diabetic hearts (98–100), which accounts for the high oxidative stress and inflammation-related DCM probably through the insufficient activation of nuclear factor-E2 related factor 2 signaling pathway (100) and sprouty homolog 1/extracellular signal-regulated kinase/mammalian target of rapamycin (SPRY1/ERK/mTOR) pathway (99). Here, MTOR is linked to familial dilated cardiomyopathy.