The exact mechanisms underlying the formation of distinct strains are not clarified, but glial-specific features of the intracellular milieu are thought to promote the selective α-synuclein misfolding and accumulation within glial cells and partially justify the different behavior of α-synuclein in MSA compared to other α-synucleinopathies (Peng et al. 2018). The gene discussed is SNCA; the disease is synucleinopathy.