Recently, Quatrana et al. [30] reported a significant upregulation of the antioxidant enzymes thioredoxin 1 (TRX1) and glutaredoxin 1 (GLRX1) in FRDA patients compared to HC, which was associated with the activation of the nuclear factor kappa B (NF-κB) p65 subunit (NF-κB p65) in fibroblasts. The gene discussed is NFKB1; the disease is Friedreich ataxia.