AQP0 plays critically important roles in maintaining lens transparency as evidenced by knockout of AQP0 in mouse and mutations of AQP0 in humans leading to congenital cataracts (Berry et al., 2000; Francis et al., 2000; Al-Ghoul et al., 2003; Zeng et al., 2013; Yu et al., 2014), with many of these AQP0 mutations resulting in cataract formation through the development of defects in plasma membrane trafficking (Shiels and Bassnett, 1996; Varadaraj et al., 2008). The gene discussed is MIP; the disease is early-onset non-syndromic cataract.