The two mutant forms (A30P and A53T) of α-synuclein, that are causative of familial, early-onset forms of PD, are autophagy substrates and pharmacological up-regulation of autophagy has been shown to enhance the clearance of these mutant proteins, resulting beneficial in the progression of several neurodegenerative disease models49. The gene discussed is SNCA; the disease is neurodegenerative disease.