Our work shows for the first time that a reduced deposition of fibrillin-1 and dysregulated expression of focal adhesion molecules by dermal B-MVECs may have an important role in SSc pathophysiology, and that the beneficial effects of CYC treatment may be due in part to the normalization of cell-matrix interactions and fibrillin-1 deposition by B-MVECs. The gene discussed is FBN1; the disease is systemic sclerosis.