In the context of DCM, hyperglycemia can directly stimulate TGF‐β1 expression, leading to phosphorylation of Smad2 and Smad3 in the cytoplasm, which then translocate to the nucleus to induce transcription of fibrosis‐promoting genes, thereby participating in myocardial fibrosis [29]. This evidence concerns the gene TGFB1 and familial dilated cardiomyopathy.