Our finding that SAHA controls Pa-LPS induced lung inflammation and neutrophil activity in Cftr+/+ mice might have interesting implications in ΔF508-CF and COPD subjects with acquired CFTR-dysfunction, where SAHA can augment CFTR function as well as control inflammatory response by CFTR dependent and independent mechanisms (Fig. 6). This evidence concerns the gene CFTR and chronic obstructive pulmonary disease.