FXN and Friedreich ataxia: These include illustrating the potential of incretin-analogue therapy by investigating the key mediators of frataxin-deficiency-induced apoptosis [22], identification of potential protein targets and mechanistic pathways of interest for epigenetic therapy [21], determination of a previously undescribed differentially methylated region upstream of the GAA repeat expansion [23] and identification of differentially expressed glycolysis pathway genes associated with FRDA, capable of rescue with lentiviral FXN expression [25].