These results indicate that, in smoking subjects, cigarette smoke promotes an inflammation and this is reflected by the increase of IL-17-producing CD4+ T-cells, whereas, in lung adenocarcinoma patients, who were classified as heavy smokers, the tumor might modify the balance to immunosuppression, mediated by the increase in the percentage of the LAP TGF-β1+ subset of CD4+CD25+CD127− Treg cells. This evidence concerns the gene IL17A and lung adenocarcinoma.