Using a mouse model of tissue specific mutation of the Foxl2 gene which recapitulated the phenotypes of the human blepharophimosis, ptosis and epicanthus inversus syndrome (BPES), it has been shown that defective development of cranial neural crest and mesodermal cell derived muscles and skeletal components would prevent eyelid closure [33]. Here, FOXL2 is linked to blepharophimosis, ptosis, and epicanthus inversus syndrome.