Kim et al. investigated the direct homeostatic relationship between these two organelles and found that neurons with GBA1 (the gene encoding the lysosomal enzyme β-glucocerebrosidase, which catalyzes the hydrolysis of glucosylceramide into glucose and ceramide) mutations found in patients with PD exhibited prolonged MLCS duration and consequent disruption of mitochondrial distribution and function (oxidative phosphorylation and ATP levels) due to defective modulation of the untethering protein TBC1D15 (Kim et al., 2021). Here, TBC1D15 is linked to Parkinson disease.