Taken together with our research, all of these observations support the idea that several familial PD gene mutations, such as A53T and A30P α-synuclein mutants (Cuervo et al., 2004), I93M UCH-L1 mutant (Kabuta et al., 2008), G2019S LRRK2 mutant (Orenstein et al., 2013) and VPS35 deficiency or mutation (Tang et al., 2015), impair the normal function of the LAMP2A translocation complex and converge at the CMA pathway, blocking CMA substrates degradation and aggravating α-synuclein accumulation and aggregation, which is thought to play a central role in PD pathogenesis (Cuervo and Wong, 2014). Here, VPS35 is linked to Parkinson disease.