The small molecule idebenone also has potential to treat Friedreich’s ataxia.435 Treatment with ferroptosis inhibitors such as SRS11-92 also inhibit Frataxin-knockdown induced human fibroblast death.432 High p53 activity reduces the transcription of SLC7A11 and the antioxidant potential of frataxin-deficient cells, therefore, inhibiting P53 activity to improve system Xc− and GSH content may be a potential therapeutic strategy to combat oxidative stress and possible ferroptosis in Friedreich’s Ataxia. The gene discussed is TP53; the disease is Friedreich ataxia.