Indeed, our results support a model whereby the heterogeneity observed both between different brain regions and between different MSA patients might be due to the differences in the cellular environment [6, 8] and to the presence of posttranslational modifications [9] and other cofactors, such as p25α [36], that may confer a selective pressure for one α-synuclein conformation over another [6]. The gene discussed is SNCA; the disease is multiple system atrophy.