Our team is working on aniridia, an autosomal dominant condition and has used a mouse model. The cornea, the eye’s first avascular and transparent optical surface, is covered by a stratified epithelium that constantly renews itself; any disruption compromises transparency and threatens vision. The tear film, rich in growth factors, protects and nourishes the corneal surface, and proteomic analysis enables global evaluation in normal and pathological states. The transcription factor PAX6 is essential for ocular development, including the lacrimal gland; its mutations cause diverse malformations and, at the corneal level, lead to progressive limbal stem cell deficiency with opacification and fibrosis, along with chronic inflammation and tear film abnormalities. Current treatments for dry eye in this context remain non-specific (artificial tears, cyclosporine, punctal plugs, scleral lenses). Identifying precise qualitative alterations of the tear film is a key step toward designing targeted therapies, such as protein-based eye drops to preserve the cornea in patients with PAX6 mutations. This project is part of a broader study aimed at evaluating the impact of a pathogenic heterozygous PAX6 mutation on the corneal and lacrimal phenotype of mice. We are interested in development, adult phenotype, and healing mechanisms following corneal injury. In this context, we performed a comparative proteomic analysis of tears in PAX6 mutant and control mice of both sexes before and after abrasion.