Furthermore, both over-expression of wild-type α-synuclein or A30P and A53T mutations of α-synuclein can inhibit autophagy [123, 124], and up-regulation of transcription factor EB (TFEB), a key autophagy modulator [125], could alleviate lysosomal damage by promoting its biogenesis, thus relieving α-synuclein associated pathology of neurodegenerative diseases [126, 127]. This evidence concerns the gene TFEB and neurodegenerative disease.