Dr. T. Michael Redmond is Chief of the Laboratory of Retinal Cell & Molecular Biology (LRCMB) and Head of the Molecular Mechanism Section, LRCMB, of the National Eye Institute (NEI), part of the US National Institutes of Health (NIH; Bethesda, Maryland). Dr. Redmond received his Ph.D. in 1983 from University College, Dublin (UCD), under the supervision of Prof. Eamonn Duke (Dept. of Zoology, UCD), following graduate training at Prof. Rosalie Crouch’s lab at the Medical University of South Carolina, Charleston, SC. He received post-doctoral training at LRCMB, NEI, investigating interphotoreceptor retinoid-binding protein (IRBP). Dr. Redmond was tenured in 1990 at NEI and began to study the gene and protein RPE65, then newly discovered by him and his group. He and his colleagues demonstrated the essential role of RPE65 in vision, that mutations in the human RPE65 gene cause Leber congenital amaurosis, a severe early onset inherited blinding disease, and that RPE65 is the crucial retinol isomerase enzyme of the vitamin A visual cycle and essential for retina vitamin A metabolism. He also collaborated in the ground-breaking effort to treat human RPE65 Leber congenital amaurosis by gene therapy in 2008. In addition, his group was the first to identify and clone the mammalian beta-carotene oxygenase enzyme, a close relative of RPE65 that catalyzes the first step in formation of vitamin A from beta-carotene by animals. In his current research on visual biochemistry, Dr. Redmond and his co-workers study the complex enzymatic mechanism of RPE65, its physiological role in maintenance of visual sensitivity and photoreceptor viability, and other research on retinal pigment epithelium metabolism.