Regarding the cellular mechanisms underlying Rimeporide’s protective effects in myocardial infarction models, Rimeporide demonstrated positive results in reducing local inflammation [38] and oxidative stress with attenuated reactive oxygen species production via NADPH oxidase and ERK1/2/Akt/GSK-3β/eNOS pathways [44,45], with no effects observed in reducing the infarct size in hearts [38,39,40]. The gene discussed is AKT1; the disease is myocardial infarction.