The authors concluded that prolonged treatment with any of the three HDAC inhibitors 106, 136 and 109 ameliorated FRDA disease-like pathology to some extent, and speculated that the apparent discrepancy in outcome with the three inhibitors could be due to differences in their potency, specificity, tissue distribution, and brain penetrance, as well as differences in dose levels and dose frequency resulting in sub maximal exposure [10]. Here, HDAC9 is linked to Friedreich ataxia.