These findings extend previous studies showing that many defects in FRDA cells in vitro and cardiac function in vivo may be reversible following reintroduction of FXN (Vyas et al., 2012) by pharmacological interventions targeting aberrant signaling processes (Rufini et al., 2015) or by reintroduction of FXN by gene therapy (Perdomini et al., 2014). Here, FXN is linked to Friedreich ataxia.