Despite that FOXL2 located on 3q23 is the only gene known to cause BPES, considering the previous reports that the whole segment of 3q21–24 contributes to BPES [28], and that FOXL2 deletion coexists with BMP15 variants in a BPES patient [13], it is reasonable to speculate that other genetic and/or epigenetic factors synergize mutant FOXL2, especially those with intact transactivation capacity, to cause and/or exacerbate BPES. This evidence concerns the gene FOXL2 and blepharophimosis, ptosis, and epicanthus inversus syndrome.