The defective embryos observed in this study might be used as suitable vertebrate disease models for linking copper overload with retinal degeneration, and the regulation signaling unveiled in this study might apply some hints for potential mechanism underlying retinal degeneration occurrence in WD patients, just like genes CERKL, SEC23A, and SEC13 function conservatively in retinal development and degeneration [20–22]. Here, SEC13 is linked to Wilson disease.