Other genetic combinations of defective subunits could also cause neurological dysfunction, with decreased dosage of m-AAA activity resulting from various mixtures of heterozygous or homozygous mutations in AFG3L2 and/or SPG7. The inheritance could appear to be either autosomal recessive and/or dominant indicating that genetic testing of AFG3L2 and SPG7 in any individuals with spastic ataxia, whether or not mitochondrial symptoms are present, may identify additional patients with m-AAA-related neurological disease. This evidence concerns the gene SPG7 and spastic ataxia.