Cataracts - cloudy lenses - are the leading cause of human blindness. How cataracts form is poorly understood although defects in crystallins, the major soluble proteins in lens fibre cells, have been implicated. Now on p. 2585, Goishi and colleagues propose that the defective expression of the protein chaperoneαA-crystallin causes the structural protein γ-crystallin to become insoluble and blocks the terminal differentiation of lens fibre cells. Together, these changes cause cataracts. The researchers began their study when they noticed that zebrafish cloche mutants, which lack blood cells and blood vessels, also have cataracts. A proteomics analysis indicated that γ-crystallin is insoluble in the cataracts of clochemutants, which led the researchers to discover that αA-crystallin is missing from cloche lenses during their development. The overexpression of exogenous αA-crystallin rescued the clochelens phenotype - one of the first times that cataract formation has been blocked in vivo. Thus, as well as providing insights into cataract formation,zebrafish cloche mutants could be used to screen for anti-cataract drugs.