On these premises, the aims of this study were to investigate 1) the possible contribution of the antiangiogenic PlxnD1/Sema3E pathway in angiogenesis disturbances and development of capillary abnormalities and digital ulcers (DUs) during SSc [23–26], and 2) if this axis might participate in the dysregulation of vascular tone control in both SSc and primary RP (pRP). This evidence concerns the gene SEMA3E and systemic sclerosis.