An intrinsic increased sensitivity to genotoxic stress in kidneys of FA patients might underlie this observation, in particular as this has been observed in mice with FANCD2/FANCI-associated nuclease (FAN1) disruption, and renal sensitivity to genotoxic stress has been reported in response to cross-linking agents and other substances, such aristolochic acid [21, 22]. This evidence concerns the gene FAN1 and Friedreich ataxia.