Generally, mutations associated with autosomal recessive forms of PD (DJ‐1, PINK‐1, PARK2, GBA‐1, ATP13A2) result in mitochondrial fragmentation and loss of complex I activity following a loss of function of their protein products (Blesa et al., 2015; Dias et al., 2013; Gegg & Schapira, 2016; Gusdon, Zhu, Van Houten, & Chu, 2012; Hayashi et al., 2009; Muftuoglu et al., 2004), indicative of an important role for these proteins in the physiological function of the mitochondrial ETC. The gene discussed is PRKN; the disease is Parkinson disease.