Several therapeutic strategies, for example, activating AMPK (AMP-activated protein kinase), ULK1 (unc-51-like autophagy-activating kinase 1), BECN1, TFEB (transcription factor EB), or ERRα (estrogen-related receptor alpha), and inhibiting the mTOR (mammalian target of rapamycin), IMPase (inositol monophosphatase), LRRK2 (leucine-rich repeat kinase 2), or c-ABL (Abelson tyrosine kinase), have been developed to enhance autophagy activity in PD models [37]. Here, ABL1 is linked to Parkinson disease.