The role of LRRK2 in regulating mitochondrial bioenergetics is exemplified in a study that showed that iPSCs derived from PD patients harboring a mutation that enhances the kinase activity of LRRK2 (G2019S), exhibited decreased basal and maximal oxygen consumption rates as well as enhanced the sensitivity of neurons to cell death induced by mitochondrial uncouplers such as valinomycin [193]. This evidence concerns the gene LRRK2 and Parkinson disease.