SDB induces a pro-inflammatory state through several mechanisms, including intermittent hypoxia, sleep fragmentation, increased oxidative stress and elevation of inflammatory mediators including tumor necrosis factor α (TNF-α), IL-6 and C-reactive protein (CRP), the concentrations of which have been correlated with SDB severity, particularly in individuals with OSA [82]. The gene discussed is CRP; the disease is obstructive sleep apnea syndrome.