For example, Huntingtin (HTT; Huntington's Disease), Frataxin (FXN; Friedreich Ataxia), and Ataxin 1/2 (ATXN1/ATXN2; Spinocerebellar Ataxias) all have GC-rich trinucleotide expansion tracks that form R-loops in vitro and associate with disease progression [58, 59]. This evidence concerns the gene FXN and juvenile Huntington disease.