The heightened state of inflammation is likely an outcome of interleukin-1 (IL-1), interleukin-6 (IL-6), interleukin-17 (IL-17), and tumor necrosis factor, which collectively perturb the equilibrium of the hypothalamic-pituitary-gonadal axis, consequently leading to a decrement in testosterone synthesis (12), Further, evidence has indicated that individuals burdened with obesity, due to augmented visceral adiposity, undergo a conversion of testosterone to estrogen within inflamed adipose tissue, thereby contributing to a depletion of testosterone levels within the organism (13, 14). The gene discussed is IL17A; the disease is obesity due to melanocortin 4 receptor deficiency.