In the complex pathophysiology of obstructive sleep apnea syndrome (OSAS), the intricate interplay of molecular mechanisms begins with the activation of Hypoxia-Inducible Factor 1-alpha (HIF-1α) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) in response to the chronic intermittent hypoxia that characterizes this condition [14,15,16,17,18]. The gene discussed is HIF1A; the disease is obstructive sleep apnea syndrome.