It has been hypothesized that vulnerability to cognitive deficits is increased in carriers of the APOE-e4 allele due to a limited response to physiological challenges (O'Hara et al., 1998; Johnson et al., 2017), and that OSA may potentiate neuroinflammatory processes associated with APOE-e4 by augmenting inflammation through hypoxia (O'Hara et al., 1998; Dewan et al., 2015; Johnson et al., 2017). The gene discussed is APOE; the disease is Cognitive impairment.