In the long term, this hyperinsulinemia, together with the loss of insulin sensitivity and the increase in the circulation of proinflammatory cytokines, promotes oxidative stress on pancreatic β cells, mitigating the function of the Nrf2 protein (transcription factor responsible for encoding antioxidant enzymes), leading to apoptosis of these cells and sustained hyperglycemia [5,69,87]. Here, INS is linked to hyperinsulinism.