The molecular pathogenesis of PD involves a complex interplay of several factors, such as impaired mitochondria, protein homeostasis, autophagy-lysosome pathway (ALP) dysfunction at the synapse, trafficking of the dopamine transporter (DAT), DA toxicity, oxidative stress, disruptions in synaptic vesicle endocytosis, autonomous pacemaking, calcium homeostasis imbalance, iron-content, extensive axonal arborization size, prion-like α-synuclein transmission, and neuroinflammation. The gene discussed is SLC6A3; the disease is Parkinson disease.