In the A53T transgenic Parkinson’s mouse model (7-8 months), nilotinib (tyrosine kinase inhibitor) can enter the brain tissue and increase the autophagic clearance of α-Syn by upregulating Beclin-1, which protects dopaminergic neurons, thereby improving the motor function of PD mice [14]. The gene discussed is BECN1; the disease is Parkinson disease.