Quantitative analysis of functional MRI data, showed that after 4 weeks of Chrdl1 treatment significantly prevented post-MI cardiac dilation and decreased the ESV (107.8 ± 35.8 μL vs 58.6 ± 20.6 μL, P < 0.01) and EDV (134.6 ± 39.5 μL vs 93.7 ± 21.1 μL, P < 0.05), improved cardiac function resulting in a higher EF (39.8 ± 11.9% vs 20.7 ± 3.8%, P < 0.001) and reduced cardiac hypertrophy evident by the reduced left ventricular mass (92.5 ± 8.2 mg vs 111 ± 19 mg, P < 0.05) compared with AAV9-Control-injected animals (Figure 2A-D). The gene discussed is CHRDL1; the disease is myocardial infarction.