FXN and Parkinson disease: As previously observed, this fold change is sufficient to rescue haploinsufficient gene dosage and disease phenotype in vivo by upregulation of protein expression of the subunit 7B of cytochrome c oxidase (cox7b) in a medaka fish model of human microphthalmia with linear skin defects (MLS) syndrome57, and rescue of endogenous defective Frataxin (FXN) expression in a cellular model of Friedreich’s ataxia58 as well as rescue of neurodegeneration and motor phenotype by enhancing endogenous Glial cell-derived neurotrophic factor (GDNF) protein expression in a mice Parkinson’s disease model59.