Moreover, the oligomers, proto-fibrils, and fibrils of α-synuclein or other misfolded proteins can form pores in a protein–membrane model inducing neuronal death through oxidative stress, energy failure, excitotoxicity, and neuroinflammation [73], providing a thorough overview of how a dysfunctional UPS can condition cellular fate and contribute to PD development. This evidence concerns the gene SNCA and Parkinson disease.