Gyrate atrophy (GA) of the Choroid and Retina was first described by Fuchs in 1896.[1] Human hereditary deficiency of ornithine aminotransferase (OAT) activity is transmitted as an autosomal recessive trait,[2] and results in 10 to 20-fold increased level of plasma ornithine and is shown to be associated with GA.[3] The initial complaint of decreasing visual acuity and night vision is followed by the appearance of sharply demarcated, circular areas of chorioretinal atrophy with hyperpigmented margins in the midperiphery of the fundus. This evidence concerns the gene OAT and Chorioretinal atrophy.