TLR4 and Friedreich ataxia: Finally, since TLR4 is modulated by ferroptosis and it is activated by the ferroptosis hallmark 4-hydroxynonenal (4-HNE) (Gargiulo et al., 2015; Hsu et al., 2022), and we previously found increased plasma levels of 4-HNE in patients (La Rosa et al., 2020b), we further analyzed the 4-HNE content in FRDA fibroblasts, to look for a potential mediator between ferroptosis and inflammation in this disease.