Notably, these changes occurred early during the evolution of obesity, prior to the development of glucose intolerance and adipocyte insulin resistance [34, 35], and contributed to activation of the p53 pathway, a key effector of the DNA damage response, which led to proinflammatory cytokine expression and AT inflammatory cell infiltration [35]. The gene discussed is TP53; the disease is obesity due to melanocortin 4 receptor deficiency.