This CRISPR-based PINK1 deficient monkey model, which exhibits obvious reduction in the protein levels of PINK1, demonstrates robust neurodegeneration in both substantia nigra and cortex, more extensive than what is found in late-onset familial PD patients with homozygous point mutation in PINK1 that can be explained by the nature of a partial loss-of-function. This evidence concerns the gene PINK1 and Parkinson disease.