Strikingly, we discovered that the TGFβ-NHEJ axis is critical for FA embryo survival; accordingly, in absence of the canonical transducer SMAD3, some DKO embryos have the capacity to rewire their intracellular signaling, engage the non-canonical ERK pathway, and transduce the apical signals coming from the extracellular TGFβ ligands. The gene discussed is SMAD3; the disease is Friedreich ataxia.