Furthermore, systemic metabolic dysregulation induced by OSA,[38] including insulin resistance and dyslipidemia, can compromise thyroid hormone synthesis, while chronic low-grade inflammation (characterized by elevated interleukin-6, tumor necrosis factor-alpha, and C-reactive protein) may directly damage thyroid tissue and inhibit deiodinase activity.[39] These pathophysiological changes collectively exacerbate thyroid dysfunction, particularly in individuals already predisposed to HT-DR, leading to greater disease severity or increased dependence on exogenous hormone replacement. The gene discussed is IL6; the disease is metabolic syndrome.