If vitamin B5 deficiency is indeed part of the pathogenesis in patients with HTT mutations, then its replacement might be a novel intervention with the potential to halt or suppress neurodegeneration itself, analogous to the effects of replacement of other B-vitamins in scenarios where a specific deficiency disorder is causative of neurodegeneration, for example vitamin B12 deficiency. The gene discussed is HTT; the disease is vitamin B12 deficiency.