The microscopic emphysema seen in the visceral pleural samples could influence the gene profile, but this is unlikely as adhesion genes as claudins, integrins and laminins were highly overexpressed, reflecting the physiological phenotype of the visceral pleura (Table 4)[10]Among the few genes over-expressed in parietal pleura were PCOLCE and PCOLCE2, encoding procollagen proteinase enhancers, important in formation of normal collagen fibrils, and thus show that the expression represents collagen-rich pleural tissue[11]. This evidence concerns the gene PCOLCE2 and pulmonary emphysema.