High P53 activity can decrease the antioxidant potential of FXN-deficient cells since, as above stated, it inhibits the transcription of the component of the cystine/glutamate antiporter, SLC7A11 [16,88]; therefore, the suppression of P53 activity in order to limit Xc system inhibition and the consequent GSH lowering could represent a good therapeutic strategy to counteract oxidative stress and likely ferroptosis in FRDA. The gene discussed is TP53; the disease is Friedreich ataxia.