Verhulst et al. believe that several hypotheses can explain the interaction between obesity and CSA: obesity leads to a decrease in the volume of the chest cavity resulting in a decrease in oxygen reserves, impaired response to hypoxia and hyperventilation, and too low ventilation due to leptin resistance leading to CSA; followed by obesity, fat reduction, or folding of the upper airway. The gene discussed is LEP; the disease is obesity due to melanocortin 4 receptor deficiency.