The mechanisms could be partially explained by excess androgens in female promoting hepatic insulin resistance by repressing NF-kB induced protein-tyrosine phosphatase 1B (PTP1B) [29], reducing skeletal glucose uptake by decreasing activation of serine/threonine-specific protein kinase AKT and glucose transporter type 4 (GLUT4) expressions [30]. The gene discussed is SLC2A4; the disease is Insulin resistance.