An in vivo active pathophysiological contribution of AECs to SSc-ILD is anyway clearly indicated by the increased serum level of AEC-secreted glycoproteins, such as surfactant protein D (SP-D) and Krebs von den Lungen 6 (KL-6),24 and by functional nuclear medicine studies showing that alveolar epithelium permeability is increased in SSc-ILD and predicts a worse prognosis.25,26. This evidence concerns the gene MUC1 and interstitial lung disease.