Current research efforts to understand the pathogenesis of HD have primarily focused on investigating abnormalities in mitochondrial dynamics, especially increased mitochondrial division, resulting in malfunctioning mitochondria, and deficits in the trafficking of axons and synaptic transmission in neurons suffering from HD.191–194 Several genes that are implicated in the ETC and mitochondrial structure, among which are Fis1, Drp1, MFN1/2, Tomm40, Opa1, and CypD, were examined in individuals suffering from stage III and IV HD. This evidence concerns the gene FIS1 and Huntington disease.