Moreover, other studies have shown that oxidative stress and reactive oxygen species (ROS) production (characteristically observed in aging and linked to insulin resistance in adipocytes) modulate other proinflammatory pathways, linking PPARγ dysfunction with inflammation [87], such as NF-κB [88], likely to contribute to altered tissue expansion and inflammation and associated age-related insulin resistance. This evidence concerns the gene NFKB1 and Insulin resistance.