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). The gene discussed is CFTR; the disease is cystic fibrosis.