FOXL2 and blepharophimosis, ptosis, and epicanthus inversus syndrome: The exact role of the poly-Ala tract in FOXL2 is unknown, but the mechanism for the molecular pathogenesis of the poly-Ala expansions in BPES has been suggested to be a result of cytoplasmic aggregation of the FOXL2 protein as well as inclusion in nuclear aggregates [16, 20–22], most often leading to BPES type II [15, 23].