PD-associated mutations in PINK1, Parkin and LRRK2 for example cause impairments of mitochondrial quality control and subsequent mitochondrial dysfunction [2] Mitochondrial-endoplasmic reticulum (ER) contact sites (MERCs) are important connections required for the proper function of mitochondria, i.e., by facilitating the exchange of metabolites, calcium and lipids between both organelles [3,4], thereby maintaining mitochondrial homeostasis. This evidence concerns the gene LRRK2 and Parkinson disease.