Allowing a more speculative interpretation, this model may intuitively posit that in the context of OSAHS alteration of sleep-related processes should be interpreted in terms of disrupted sleep homeostasis evolving due to intermittent airway obstruction, consequent hypoxia, and arousals and also via the alteration of the intertwining circadian regulatory processes reflected by the complex interaction between excessive daytime sleepiness and the irisin/BDNF axis. This evidence concerns the gene BDNF and obstructive sleep apnea syndrome.