The most recent work on miRNA therapeutics for FRDA has done by Bandiera et al. [4] by transfecting HEK-293 cells with hsa-miR-124 mimics, where the overexpression of the later was correlated with a down-regulated FRDA-3-UTR haplotype, which expands the FRDA risk haplotype to the 3′-UTR. This evidence concerns the gene FXN and Friedreich ataxia.