Since cell culture studies demonstrated that St-PGA-CL-BDMC prevented NF-κB/p65 nuclear translocation and the subsequent transcription of NF-κB target genes involved in the pathogenesis of AKI (Fig. 4), we explored the impact of St-PGA-CL-BDMC in kidneys from mice with FA-AKI in this regard. The gene discussed is NFKB1; the disease is Friedreich ataxia.