AKT1 and metabolic dysfunction-associated steatotic liver disease: SIL, as an insulin sensitizer, could generate a moderate increase of the expression of glucose transporter type 4 (GLUT4), thereby ameliorating the IR via insulin receptor substrate 1 (IRS-1)-PI3K-Akt pathway.[27] It was reported that SIL had shown encouraging effects in reducing TNF-ɑ, IL-1β, and IL-6 in animal models.[28,29] Patients with NAFLD benefited from SIL scavenging oversupplies of fatty acids and oxidative stress.