This “vascular hypothesis” of COPD has been supported by the results of a recent study in which the expression of both vascular endothelial growth factor (VEGF) and its receptor were shown to be decreased in lung tissue from patients with COPD.4 Besides, cigarette smoke disrupts components of VEGF165 and its receptor VEGFR2 with decreased expression of VEGF and its receptors in the lungs of rats and humans.5 The pathogenesis of COPD may therefore be more complex and multifactorial, resulting from an interaction between genetic, environmental, cigarette smoke and angiogenesis factors. This evidence concerns the gene KDR and chronic obstructive pulmonary disease.