Obesity is a risk factor for diabetes due to its association with chronic inflammations; Li et al. revealed that the anti-inflammatory effect of OA on obesity-induced inflammation in mice is presumably caused by the suppression of interferon gamma/lipopolysaccharide (IFN-γ/LPS)-induced M1 phosphorylated kinases by reducing ROS expression, hence inhibiting the MAPK signaling and NLRP3 inflammasome formation (Figure 11) [158]. This evidence concerns the gene IFNG and obesity due to melanocortin 4 receptor deficiency.