Conversely, inhibition of the TGF-β pathway through silencing of the SMAD3 gene in FA mice and human cells modulates the expression of DNA repair genes in favor of homologous recombination (HR) over NHEJ, resulting in increased growth of hematopoietic progenitors and rescue of bone marrow failure [29]. The gene discussed is TGFB1; the disease is Friedreich ataxia.