Indeed, when primary cortical neurons are exposed for 12 h to camptothecin in order to mimic the chronic genotoxic oxidative stress occurring in neurodegenerative diseases (Lin and Beal, 2006), a significant mitochondrial elongation with a suppressed expression of fission protein Drp1 and Parkin is clearly detectable in these in vitro cultures, in contrast to the opposite effect of other forms of stress (i.e., staurosporine and glutamate treatment) which are able to induce a marked fragmentation of these organelles. Here, PRKN is linked to neurodegenerative disease.