TNF-α and IL-6 stimulate both the c-Jun N-terminal kinase (JNK) and the inhibitory-κB kinase (IKK)/nuclear factor-κB (NF-κB) pathways through conventional receptor-mediated mechanisms, resulting in overexpression of possible inflammatory mediators that can eventually contribute to insulin resistance (Figure 1) [29-33]. This evidence concerns the gene IL6 and Insulin resistance.