Thus, the appearance of 14–3-3, mitochondrial dysfunction, Huntington’s disease, neuroinflammation, and synaptogenesis signaling as the common toxicity pathways for α-synuclein and other neurotoxic proteins amyloid beta, tau, and Huntingtin suggest that these pathways are likely activated as a result of the host cell stress response or secondary non-specific response to the toxicity and immunogenicity of α-synuclein rather than as a direct consequence of the α-synuclein toxicity. This evidence concerns the gene MAPT and Huntington disease.