Mechanistically, 1938 mitigates myocardial injury by activating the PI3Kα/AKT pathway implicated in cardioprotection.27,30 We confirmed that 1938 treatment increased the phosphorylation of both AKT (Figure 4A and B) and eNOS (Figure 4A and D) in DM mice. The gene discussed is AKT1; the disease is diabetes mellitus.