CDC42 and Familial exudative vitreoretinopathy: The genetic ablation of Rac1 in the limb bud ectoderm of mouse embryos would disrupt the canonical Wnt signaling.[13] Lutze et al have also described noncanonical Wnt-signaling for the differentiation of lymphatics and the extension of lymphangiogenesis via Rac and c-Jun N-terminal kinase, suggesting that Rac has effects on the Wnt signaling.[14] Therefore, we proposed that genes ARHGAP31 and DOCK6 may interact with Wnt signaling through Rho GTPase Rac1 and Cdc42, which plays important role in the pathogenesis of FEVR.