This may include pharmacological agents that address the primary defect of frataxin deficiency by increasing FXN gene expression and/or frataxin protein such as those identified in this study, HDAC inhibitors [72]–[74], erythropoietin [75]–[77], PPAR-γ agonists [66] or IFNγ [78], and those directed at secondary effects, such as antioxidants and iron-chelators. Here, HDAC9 is linked to hyperinsulinemic hypoglycemia, familial, 4.