Congenital cataract occurs in 90–95% of diabetic rat fetuses. The pathogenetic mechanism is triggered by fetal hyperglycemia and presents the following steps: (1) a high glucose concentration in the lens; (2) reduction of glucose to sorbitol by aldose reductase; (3) accumulation of sorbitol into the fibers of the lens creating a hyperosmotic effect, leading to (4) an infusion of liquid into the fibers, which (5) become hydropic and degenerate (vacuolization). This series of manifestations might also occur in fetuses of pregnant diabetic mothers. Post birth glycemia diminishes rapidly, and this favorable condition which decreases vacuolization is perhaps the reason why such degeneration has not yet been observed. Since the fibers of the lens are permanent cells, damage in the fetal period might later bring about negative consequences. We hope that someone will study whether this ocular pathology occurs in human infants born to diabetic mothers.