Nevertheless, by considering that previous studies did not distinguish between proangiogenic VEGF(165) and antiangiogenic VEGF(165)b isoforms, originated by alternative splicing in the terminal exon of VEGF pre-RNA, Manetti et al. [39] have observed that a switch from proangiogenic to antiangiogenic VEGF isoforms may be responsible for the inefficient angiogenic response in SSc. Here, VEGFA is linked to systemic sclerosis.