Reprogramming FRDA fibroblasts in the presence of sodium butyrate, an HDAC class I inhibitor, or tranylcypromine, a lysine-specific demethylase 1 inhibitor, significantly increased FXN expression and was associated with the correction of some of the repressive histone modifications at the FXN locus in derived FRDA iPSCs. Here, FXN is linked to Friedreich ataxia.