Transgenic overexpression of IFN-γ in the lungs induces production of matrix metalloproteinases by macrophages and development of emphysema in a murine model[45], Similarly, a central role for TNF-α in smoking-induced emphysema development is well-supported by data from murine models[46-48], likely reflecting in part the ability of TNF-α to activate endothelial cells to increase recruitment of inflammatory cells. This evidence concerns the gene TNF and pulmonary emphysema.