Serine, cysteine, and/or metalloproteinase classes have been reported as the proteases most likely to be involved in the pathogenesis of chronic obstructive pulmonary disease (COPD) and may be the reason for the successful employment of protease inhibitors, as reported for the inhibitors applied in experimental in vivo models of elastase-induced lung injury [84,85] and an asthma model [86], with a reduction in the expression of TNF-α, MMP-9, MMP-12, TIMP-1, eNOS, and iNOS cells in the airways and alveolar walls with inhibitor treatment. This evidence concerns the gene TIMP1 and chronic obstructive pulmonary disease.