We may hypothesize that during the course of SSc, a pathological environment enriched in TGF-β may contribute to increased EGFL7 expression, thus influencing vascular remodeling, while at later stages other factors may contribute to a reduction of EGFL7 expression levels which in combination with the pro-fibrotic environment induced by TGF-β and induction of anti-angiogenic growth factors such as PEDF31 results in the severe vasculopathy observed at later stages of SSc. Here, TGFB1 is linked to systemic sclerosis.