It cuts α‐Syn N103 and accelerates its fibrillization in PD.[17] Remarkably, α‐Syn N103 stimulates monoamine oxidase (MAO) enzymatic activity, leading to DOPAL escalation and AEP augmentation in PD.[18] It also fragments UNC5C, a netrin‐1 receptor, at the N467 and N547 residues, facilitating both AD and PD onset.[19] DA neurons expressing Sox6 and ALDH1A1,[4, 20] located in the ventral SNpc, are selectively vulnerable in PD. Here, ALDH1A1 is linked to Parkinson disease.