These findings were then validated in a zebrafish vhl−/− knockout and a mouse model of Leigh syndrome caused by disruption of the Ndufs4 gene, encoding a subunit of mitochondrial Complex I. This study poses a possibility of hypoxia induction as mitochondrial disease therapy by potentially triggering an adaptive response mechanism(s) that decreases the body’s reliance on oxidative respiratory rate [65]. This evidence concerns the gene NDUFS4 and Leigh syndrome.