Considering the cardioprotective and beneficial impact of netrin-1 in myocardial infarction, we hypothesized that overexpression of netrin-1 in mice will prevent diabetes-induced VED by increasing NO production, limiting oxidative stress and preventing activation of inflammatory and apoptotic mediators through the DCC-ERK1/2 pathway. The gene discussed is NTN1; the disease is myocardial infarction.