Profiling 18 sporadic HNSCC cell lines revealed that 53% of them showed increased chromosomal breakage with exposure to mitomycin C or cisplatin, ICL-generating agents, which is a pathognomonic feature of FA, albeit only a subset of them had identifiable pathogenic mutations in FA genes or promoter hypermethylation of FANCF [67]. Here, FANCF is linked to Friedreich ataxia.