MST1 and neuroblastoma: To verify the role of Mst1/2 in response to neurotoxic conditions, we next examined the effect of Mst1/2 knockdown in SH-SY5Y human neuroblastoma cells treated with MPP+, a well-known neurotoxin that induces mitochondrial dysfunction by inhibiting complex I. Similar to the findings in Drosophila, Mst1/2 double knockdown in SH-SY5Y cells significantly reduced mitophagy induction (approximately 40%) and further decreased mitochondrial membrane potential and cell viability upon MPP+ treatment (approximately 13% and 13%, respectively) (Fig. 6a–c, Supplementary Fig. 6a).