Thus, we assessed (i) whether adjunctive administration of physiological concentrations of E2 after infarction can result in attenuated ventricular remodelling, (ii) whether the PI3K/Akt/eNOS axis plays a role in mediating remodelling, and (iii) whether GPER and membrane ERα modulate the activities of eNOS in a rat MI model. The gene discussed is GPER1; the disease is infarction.