Finally, the significant overproduction of profibrotic factors such as IL-17, GM-CSF, and ET-1 in scleroderma patients without gastritis compared with those presenting atrophic gastritis, and the significant reduction of TGF-β, IL-6, and IL-2 in atrophic gastritis compared with patients without gastric involvement and with superficial gastritis are potentially conflicting with expectations. This evidence concerns the gene TGFB1 and scleroderma.