Both in vitro and in vivo studies have demonstrated that IFN-γ can upregulate Frataxin levels by modulating Frataxin gene transcription, which helps improve sensory and motor deficits in Friedreich’s ataxia mouse models.815 IFN-γ enhances the expression of Nrf2 and manganese-dependent superoxide dismutase in Friedreich’s ataxia cells, activating the non-canonical Nrf2 pathway via p21. Here, IFNG is linked to Friedreich ataxia.