Indeed, the identification of loss-of-function mutations in PINK1 and PRKN – which encode PINK1 (a mitochondrially targeted serine/threonine kinase) and Parkin (a cytosolic E3 ubiquitin ligase), respectively – as a cause of autosomal recessive, early-onset PD has cemented mitochondrial disruptions as a major contribution to PD [10,11]. Here, MARK2 is linked to Parkinson disease.