Partial deletion and overexpression of IGF-I under defective conditions reduce myocardial contractility, alter sensitivity to Ang II, promote interstitial fibrosis, increase extracellular matrix collagen secretion, and change the expression patterns of genes related to cardiomyocyte calcium dynamics and cardiac structural proteins, confirming IGF-I’s role in myocardial fibrosis (González-Guerra et al., 2017). The gene discussed is AGT; the disease is Myocardial fibrosis.