In states of metabolic dysfunction such as obesity and diabetes, ROS levels become exceedingly high, and when compounded with POPs exposure, innate antioxidant defense mechanisms become overwhelmed with increased levels of ROS from the activation of RAGE/NF‐κB signaling.26, 32 Thus, decreased SOD expression in diabetic‐POPs treated animals may have dampened the cardioprotective mechanisms needed to offset POPs‐mediated oxidative and inflammatory stressors. Here, NFKB1 is linked to obesity due to melanocortin 4 receptor deficiency.