When evaluating the possible association of sNRP1, Sema3E, and Slit2 with different SSc clinical phenotypes, none of the three circulating molecules was found to be significantly different according both to the SSc cutaneous subset (i.e., limited cutaneous SSc and diffuse cutaneous SSc) and to the distinct autoantibody pattern (data not shown). This evidence concerns the gene SLIT2 and systemic sclerosis.