TNF and Friedreich ataxia: In the ICI-treated cohort, we found that the TNFα-MT group had a significantly higher number of mutations in the double-strand break (DSB), Fanconi anemia (FA), homologous recombination (HR), nucleotide excision repair (NER), nonhomologous end joining (NHEJ), single-strand break (SSB), and merged DDR pathways than the TNFα-WT group (all P <0.05; Figure 3A).