Surprisingly, no CTGF signal was detected in the endothelial cells, however, the acinar cells of DC-associated sweat glands were positive for this molecule, which suggest that sweat glands might have an hitherto unrecognized role in the development of DC lesions by providing proproliferative profibrotic CTGF signaling to the DC tissue (Fig. 5a, b). This evidence concerns the gene CCN2 and dyskeratosis congenita.