PARP1 and Friedreich ataxia: Previous studies showed that non-homologous end joining (NHEJ), homologous recombination (HR) via the Fanconi anaemia (FA) pathway, and poly(ADP-ribose) polymerase 1 (PARP1)–dependent DNA repair are involved in the repair of AzadC-induced DNA lesions (26, 27, 28).