Although the underlying mechanisms for the exertional desaturation associated with mortality in patients with COPD are not fully established to date, the accompanying hypoxia and hypoxemia may promote bacterial infections [31], enhance the activation of hypoxia-inducible factors (HIFs) and nuclear factor (NF)-κB [32], and propagate systemic inflammation or increase the number of recurrent exacerbations [32,33]. This evidence concerns the gene NFKB1 and chronic obstructive pulmonary disease.