Mutations in the OPA1 gene were at first considered to be reasonable candidates for autosomal dominant optic atrophy (ADOA) because the defective The OPA1 gene product may cause a derangement in mitochondrial metabolic function, including respiratory deficiency, which may be involved in the degeneration of retinal ganglion cells and atrophy of the optic nerve [45], [46], [47].The similarities between the clinical phenotypes and the finding that OPA1 is expressed in the optic nerve made OPA1 an excellent candidate susceptibility gene for POAG, or specifically for NTG [48], [49], [50]. Here, OPA1 is linked to autosomal dominant optic atrophy.