Using the occurrence of DRG vacuoles as a marker of FRDA disease pathology in our YG8R mice, we have shown that, as with restoration of the aconitase deficit, the HDAC inhibitor that produced the most significant improvement in DRG neuronal cell pathology is 109, the HDAC inhibitor that produced the most significant increase in frataxin expression. Here, HDAC9 is linked to Friedreich ataxia.