ATR and Friedreich ataxia: To detect, signal, and repair these lesions, cells rely on a complex response that typically gets triggered when the replication machinery encounters the ICL and involves the precise and coordinated effort of multiples pathways, including the Fanconi anemia (FA), nucleotide excision repair (NER), and the homologous recombination (HR) repair pathways, alongside the ATR serine/threonine kinase (ATR) checkpoint signaling pathways (1).