FOXL2 and blepharophimosis, ptosis, and epicanthus inversus syndrome: Among all genetic defects found in BPES, an estimated 72% of cases are due to intragenic FOXL2 mutations [12]; 2% of cases involve cytogenetic rearrangements containing unbalanced translocations and interstitial deletions of 3q23 [13]; about 12% of BPES cases result from deletions involving partial or whole FOXL2 gene deletion and contiguous gene deletion, including FOXL2 and adjacent gene(s) [13]; and about 5% of cases involve regulatory deletions outside the FOXL2 gene [14].