Increased RBP4 levels cause insulin resistance, in part by activating adipose tissue APCs that induce Th1 polarization and inflammation, and RBP4-induced activation of macrophages and antigen presentation to CD4T Cells are partially dependent on JNK signaling, resulting in increased levels of TNF and IFN-γ and further increase inflammation [27]. This evidence concerns the gene TNF and Insulin resistance.