The protective role of αA-crystallin reported in our study is consistent with multiple previous studies reporting that αA-crystallin upregulation plays a protective role in the suppression of photoreceptor apoptosis associated with intraocular inflammation [25], experimental autoimmune uveitis [26], and a Rpe65−/− mouse model of Leber congenital amaurosis [27]. The gene discussed is RPE65; the disease is inflammatory response.