Grafting experiments with this fibrin-bound VEGF variant demonstrated controlled growth of morphologically normal blood vessels.26 Based on this evidence, we hypothesised that local administration of VEGF121-fibrin and consequent cell demanded release of VEGF from the fibrin matrix should overcome the uncontrolled VEGF expression found in SSc, and induce sufficient angiogenesis to heal and prevent ischaemic ulcers. Here, VEGFA is linked to systemic sclerosis.