Moreover, both overexpression and direct pharmacological activation of TFEB protect against accumulation of aSyn/tau and associated neurodegeneration in several murine and in vitro models [5, 16, 27, 66], suggesting TFEB could represent a potential therapeutic target for PD and other proteinopathies, such as DLB and Alzheimer’s disease [30, 33, 53, 66]. The gene discussed is TFEB; the disease is Alzheimer disease.