Thus, we hypothesize that increased SAA1 production may inhibit insulin-induced Akt phosphorylation via stimulation of PTEN expression upon activation of TLR2/4 and NF-κB pathway, resulting in the attenuation of insulin-induced GLUT4 translocation, glucose uptake in granulosa cells and IR development in granulosa cells in PCOS. Here, AKT1 is linked to polycystic ovary syndrome.