Although inhibition of mitochondrial fission has been proposed as a therapeuticapproach for HD, we find that removal of Mff, a mitochondrial fission factor,exacerbates the neurological phenotypes ofHDR6/2 mice.Therefore, ourresults indicate that a deeper understanding of mitochondrial dynamics in HD isrequired before mitochondrial fission can be considered a therapeutic avenue forHD. This evidence concerns the gene MFF and Huntington disease.