An animal study demonstrated that activation of the RAGE/NF-κB pathway induces neuronal degeneration, whereas activation of the S100B/RAGE/NF-κB pathway leads to reactive gliosis in the sleep apnea model of intermittent hypoxia exposure [19] Braga et al. [13] showed that there was an increase in S100B protein levels in OSA patients compared to a control group, but S100B did not correlate significantly with AHI score or minimum SpO2. Here, NFKB1 is linked to sleep apnea syndrome.