In conclusion, systemic gene therapy with the rAAV9 vector induced robust, durable, and cardiac-specific transgene expression, and rAAV9-mediated Wnt11 expression was associated with significantly greater cardiac performance, significantly less fibrosis, and profound improvement in survival after MI, presumably via suppressed infiltration of inflammatory cells including macrophages and suppressed gene expression of inflammatory cytokines. The gene discussed is WNT11; the disease is myocardial infarction.