Experiments on SH-SY5Y neuroblastoma cells and primary rat dopaminergic midbrain neurons revealed that stimulators such as the dopaminergic neurotoxin 6-OHDA, rotenone, and MPP+ induced the overexpression of DRP1, which triggered their translocation from the cytoplasm to mitochondria and bound to Bax to co-promote mitochondrial fission, in which DRP1 initiated the GTP hydrolysis pathway and promoted the continued fission of mitochondrial membranes [74,75,76,77]. The gene discussed is DNM1L; the disease is neuroblastoma.