The mechanisms underlying contributions of proinflammatory T cells (mainly CD4+ Th1 and effector CD8+ T cells) to insulin resistance may include direct adverse effects of these T cells or T cell cytokines such as IFN-γ on metabolic functions and insulin sensitivity in adipocytes or skeletal muscle through the JAK/STAT1 pathway (24, 65, 70) and T cell effects on other immune cells such as macrophages, which also play important roles in metabolic functions including insulin resistance. This evidence concerns the gene STAT1 and Insulin resistance.