Fibrosis is a key mechanism in the progression of DCM, and several miRNA are involved in this process, like miRNA-208, which is connected to an increase in myocardial collagen volume and worse clinical outcomes in DCM patients, and MiRNA-218-5p, which stimulates TGF-β and promotes a profibrotic effect [73,74]. The gene discussed is TGFB1; the disease is familial dilated cardiomyopathy.