Although multiple lines of evidence indicate that chronic oxidative stress occurs by CHCHD2 loss, overexpression of SOD1 and DJ-1 or removal of DJ-1 did not affect dCHCHD2 phenotypes, which strongly suggests that oxidative stress is only part of the pathogenesis of PD that is linked to CHCHD2. The functional difference between SOD1/DJ-1 and 4E-BP is that the latter regulates mitochondrial functions and proteostasis in addition to upregulation of anti-oxidative proteins such as anti-oxidant GST-S1 (refs 11, 12, 17, 31). Here, SOD1 is linked to Parkinson disease.