Notably, codon optimized versions of OPA1 isoform 1 and 7 were generated and both isoforms were shown to modulate mitochondrial bioenergetics in cell models of OPA1 dysfunction and protect spatial visual function and PhNR responses in a chemically induced mouse model displaying many of the morphological and functional phenotypes of optic neuropathy, although the OPA1 based therapy only provided a trend toward protection of RGCs. The gene discussed is OPA1; the disease is optic nerve disorder.