Finally, given that β-synuclein can attenuate α-synuclein toxicity in vivo[46], [47], [48], [49], it is attractive to propose that regulation of endogenous β-synuclein expression and Akt activation may be a significant factor in the transgenic animal models of α-synucleinopathy and in human α-synucleinopathies. This evidence concerns the gene SNCB and synucleinopathy.