SLIT2 and systemic sclerosis: These processes were mediated by reduced VEGF-165-stimulated phosphorylation of the Src family of nonreceptor tyrosine kinases (SFKs) and subsequent activation of Rac1 [8] (Figure 1A).Recently, the expression of Slit2 and Robo4, but not of Robo1, was reported to be increased in forearm skin biopsies from patients with systemic sclerosis, and the Slit2/Robo4 axis interfered with angiogenesis by inhibiting Src kinase phosphorylation [26].