FOXE3 (forkhead box E3) is a transcription factor essential for lens development and eye morphogenesis. The protein functions as a DNA-binding transcription factor that controls lens epithelial cell growth through regulation of proliferation, apoptosis, and cell cycle progression 1. During lens development, FOXE3 is expressed from the start of lens placode induction and becomes restricted to anterior proliferating cells when lens fiber differentiation begins 1. The protein is crucial for lens vesicle closure and subsequent separation from the ectoderm, promoting survival and proliferation while preventing premature differentiation in lens epithelium 1. FOXE3 mutations cause severe ocular developmental anomalies with distinct genotype-phenotype correlations. Recessive mutations typically result in congenital primary aphakia, sclerocornea, and microphthalmia, while dominant mutations cause anterior segment dysgenesis 23. The sclerocornea-microphthalmia-aphakia complex represents the most severe phenotype, characterized by absent lens, opaque cornea, and small eyes 34. Comprehensive mutation analyses have identified over 50 variants in FOXE3, establishing it as a major gene for congenital eye malformations 5. These findings demonstrate FOXE3's critical role in orchestrating early eye development and maintaining lens epithelial homeostasis.