VEGFA and systemic sclerosis: Indeed, it has been demonstrated that through an alternative splicing in its terminal exon, the VEGF primary transcript can produce at least six isoforms, one of which is represented by the anti-angiogenic VEGF165b splice variant [82,83,84], and that in SSc patients the increase in VEGF is the result of a significant rise in the anti-angiogenic VEGF165b isoform instead of the corresponding pro-angiogenic VEGF165 [85,86].