Yu et al. [123] demonstrated a reduction in miR-133a levels in the infarct border zone after MI in mice and that forced miR-133a expression improves cardiac function and reduces fibrosis, providing evidence that the expression of TGF-β1, CTGF (connective tissue growth factor), Col1α1, Col1α3, and α-SMA were decreased (Figure 2) [123]. The gene discussed is COL1A1; the disease is myocardial infarction.