In this sense, while CCN2 inhibition using a monoclonal antibody attenuates left ventricular remodeling and dysfunction in pressure overload-induced heart failure [21], CCN2 knockout does not affect cardiac hypertrophy and fibrosis formation upon chronic pressure overload [22], and cardiac-restricted overexpression of CCN2 attenuates left ventricular remodeling after myocardial infarction [23]. The gene discussed is CCN2; the disease is myocardial infarction.