We assume that the pre-existing chronic inflammation in obesity may enhance the Th1/Th17 response and the imbalance in favor of CD8+ T cells over T-reg cells in the bloodstream, potentially increasing the risk of autoimmune disease in the general population and of irAEs in patients treated by immunotherapy [46], with the abolition of the inhibition of the negative immune checkpoint increased in obese patients, as previously reported. The gene discussed is CD8A; the disease is obesity due to melanocortin 4 receptor deficiency.