Such bacterially driven regulation of PAF signaling might be overcome by a therapeutic increase of PAF levels at the site of infection through PLA2 targeting (82), which in turn, might also dampen free AA release in COPD patient lungs, therefore limiting selection against FadL function during NTHi pathoadaptation (for a model, see Fig. 9). This evidence concerns the gene PCLAF and chronic obstructive pulmonary disease.