Although a direct mechanistic pathway can be definitively established between EPO and NADPH oxidase in the context of hypoxia-induced CNS susceptibility, this study suggests that efforts aiming to increase either EPO expression or the activation of EPO receptors in the CNS may be a promising target for OSA treatment, especially in stopping the progression, and potentially reversing the well known OSA-associated cognitive and behavioral morbidities. Here, EPO is linked to obstructive sleep apnea syndrome.