The first connection between CMA and PD was established in 2004, where monomeric and dimeric wild-type α-synuclein species were shown to be CMA substrates, whereas the A30P and A53T PD-linked mutant α-synuclein forms bound more tightly to LAMP2A, CMA’s specific receptor, but were not up taken and degraded within lysosomes, thus becoming toxic by inhibiting the CMA-mediated degradation of other cytosolic substrate proteins (Cuervo et al., 2004). Here, SNCA is linked to Parkinson disease.