FXN and Friedreich ataxia: The increase of FXN mRNA was also demonstrated in FA fibroblasts treated with different NRF2 inducers [77], thus strongly suggesting that intervening in the restoration of the FA-induced defects on NRF2 molecular circuitry could lead to the rescue of FA primary defect, (i.e., frataxin protein deregulation), as well as to re-balance the secondary hit (the increased oxidative stress).