Further supporting the α-syn species toxicity, CMA inhibition by either PD-linked α-syn mutants or dopamine-modified wild-type α-syn results in an accumulation of α-syn, but also of undegraded CMA-substrates, involved for instance in the regulation of neuronal survival through the degradation of the neuronal survival factor myocyte enhancer factor 2D (MEF2D; Yang et al., 2009). This evidence concerns the gene MEF2D and Parkinson disease.