Based on its role in retinal angiogenesis during development, mutations in TSPAN12 or large deletions of TSPAN12 cause familial exudative vitreoretinopathy in human (Nikopoulos et al., 2010; Yang et al., 2011; Seo et al., 2016), in contrast, the anti-TSPAN12 antibody, which inhibits ECs migration and tube formation, ameliorates vasoproliferative retinopathy via suppressing β-Catenin signaling in rodent models of retinal neovascular disease (Bucher et al., 2017). This evidence concerns the gene TSPAN12 and exudative vitreoretinopathy.