Our data suggest that DOX induces an increase in mitochondrial ROS formation resulting in early ubiquitination of FXN protein by activating E3 ligase at the current DOX as inferred by other studies demonstrating mechanisms for FXN turnover in FRDA patients (Landré et al., 2014; Rufini et al., 2014). The gene discussed is FXN; the disease is Friedreich ataxia.