Further clarification of ALDH3A1’s role in the cornea has been provided by gene-knockout studies in which genes encoding ALDH3A1 were removed from the mice genome. It was found that ALDH3A1-null mice exhibited lower proteasome activity, higher rates of protein degradation/oxidation, and higher GSH, 4HNE and malondialdehyde protein adduct levels—all of which contributed to the development of cataracts and opacities in the subcapular regions of the cornea within one month of age.[23] These observations on ALDH3A1-null mice reaffirm that ALDH3A1’s role extends beyond enzymatic metabolism; encompassing functions in maintenance of the structural integrity and transparency of the cornea.