When the PTEN was overexpressed, insulin signaling effects were inhibited, resulting in decreased RAC-alpha serine/threonine-protein kinase (AKT) activity and solute carrier family 2, facilitated glucose transporter member 4 (GLUT4) translocation to the cell membrane, which consequently contributed to insulin resistance and progression of non-alcoholic fatty liver disease [21,22,23]. The gene discussed is INS; the disease is metabolic dysfunction-associated steatotic liver disease.