Overexpression of CTRP9 promoted hypertrophic myocardial remodeling and dysfunction after TAC in response to pressure overload, while TAC was alleviated in CTRP9 knockout mice, suggesting that upregulation of CTRP9 promotes maladjusted cardiac remodeling and left ventricular dysfunction (Appari et al., 2017). The gene discussed is C1QTNF9; the disease is persistent truncus arteriosus.