Additionally, plasma and myocardial expression of CTRP3 in mice was significantly decreased following myocardial infarction (MI), whereas CTRP3 replenishment improved mouse survival, restored cardiac function, attenuated myocardial hypertrophy, decreased the number of myofibroblasts post-MI [21, 22], and may be beneficial for attenuating vascular remodeling [23]. The gene discussed is C1QTNF3; the disease is myocardial infarction.