Cardiomyocytes‐specific knockdown of Decr1 preserved cardiac function (+41% for EF, p < 0.0001; +24% for FS, p = 0.0052), inhibited cardiac hypertrophy (−34%, p < 0.0001), fibrosis (−69%, p < 0.0001), apoptosis (−56%, p < 0.0001) and oxidative damage (−59%, p < 0.0001) in DCM mice, while cardiomyocytes‐specific overexpression of Decr1 aggravated DCM (−28% for EF, p = 0.0347; −17% for FS, p = 0.0014). The gene discussed is DECR1; the disease is familial dilated cardiomyopathy.