Our data are consistent with the model that CTCF depletion in the 5′UTR of the FXN gene in FRDA patients results in reduced FXN transcription via heterochromatin formation involving the critical +1 nucleosome, which offers a plausible mechanism for transcriptional silencing of the FXN gene, and is consistent with the observed transcriptional reactivation via administration of HDAC inhibitors [6]. The gene discussed is FXN; the disease is Friedreich ataxia.