A fact that argues in favor of the role of α-synuclein/lipid interaction in the etiopathogenesis of synucleinopathies is that all missense mutations responsible for familial PD are localized in the 11-residue repeat domain that has membrane-binding properties; indeed, these mutations alter the lipid binding properties (Jo et al., 2002; Fares et al., 2014; Ghosh et al., 2014; Robotta et al., 2017). Here, SNCA is linked to synucleinopathy.