For example, nonreceptor tyrosine kinase Abelson (c-Abl) is increased in PD patients and PD animal models, pharmacological inhibition of c-Abl inhibits GSK3β activity, and thus activates TFEB-mediated lysosomal biogenesis to promote α-synuclein degradation and alleviates PD pathology [97]. The gene discussed is GSK3B; the disease is Parkinson disease.