In acute and/or chronic CS exposures, rhCC16 treatment in WT and Cc16–/– mice reduced lung NF-κB activation and contributed to reduced macrophage and/or PMN counts, leading to reductions in Mmp-9 and Mmp-12 expression levels in the lungs (as these cells are sources of these proteinases) and reductions in emphysema. This evidence concerns the gene MMP12 and pulmonary emphysema.