The molecular pathogenesis of these repeat expansion diseases is considered to include loss of host gene function as in fragile X syndrome and Friedreich ataxia, production of toxic RNAs as in DM1 and C9orf72-ALS/FTD, and production of toxic polypeptides as in polyglutamine diseases such as HD and several SCAs. This evidence concerns the gene C9orf72 and Huntington disease.