A novel G9053A mutation was identified in four T2DM patients with cataracts, all carrying the A3243G mutations [10], and has been reported in silico to disrupt the proton channel of ATP synthase through the S167N substitution in the ATPase6 gene, impairing ATP production and contributing to T2DM and cataract pathophysiology [18]. The gene discussed is MT-ATP6; the disease is cataract.