Fusion of TAT peptide to full-length FXN protein [197] or to mature FXN protein harboring another MTS signal [198] drove the fusion proteins to the mitochondria of cells derived from FRDA patients as well as in FXN-deficient neurons and increased cell survival, decreased neuritis degeneration, and reduced apoptotic markers [197,198]. This evidence concerns the gene FXN and Friedreich ataxia.