In this study, lenses of Epha2+/− mice, despite accumulation of the fusion protein in cells, remained clear when wild-type EPHA2 protein produced by the normal allele was localized to the cell membrane (at 18 weeks of age), and developed severe cortical cataracts when it was lost from the cell membrane (at 45 weeks of age). Here, EPHA2 is linked to cortical cataract.