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. This evidence concerns the gene CDC42 and exudative vitreoretinopathy.