The contribution of Slit2 to SSc-related vascular dysfunction has been demonstrated in a work published by our group, in which circulating Slit2 levels were found to be significantly increased in sera from both SSc and VEDOSS patients with respect to controls, with higher levels being specifically correlated with the presence of microvascular abnormalities in VEDOSS subjects, suggesting that Slit2 could reflect the presence of peripheral vascular impairment since the very early phase of SSc [122]. This evidence concerns the gene SLIT2 and systemic sclerosis.