2010; Gegg and Schapira 2011). The mitochondrial dysfunction associated with aberrant PINK or parkin function is likely, at least in part, to increase the accumulation of damaged mitochondria. Indeed, impairment of oxidative phosphorylation in PINK1‐deficient SH‐SY5Y neuroblastoma cells was reversed by over‐expressing parkin and restoring autophagic flux (Gegg et al. 2010). However, it should be noted that constitutive knockdown (KD) of PINK1 expression in SH‐SY5Y cells has been reported to activate mitophagy in the absence of CCCP (Dagda et al. 2009). The gene discussed is PINK1; the disease is neuroblastoma.