Indeed, such epigenetic therapy would have two distinct advantages in FRDA: (a) a negative immune response to increased frataxin protein would be unlikely, since the body is already exposed to residual frataxin levels and (b) only a slight increase in frataxin levels may be needed to have a significant clinical effect, since heterozygous FRDA carriers are phenotypically normal. The gene discussed is FXN; the disease is Friedreich ataxia.