Regarding PD therapies, optimizing the function of MUL1 is likely to be beneficial for PINK1/PARKIN patients; upregulating MUL1 may rescue the pathology due to lack of PINK1 or PARKIN. In contrast, downregulating MUL1 and/or mutations in MUL1 may lead to disruption of this compensatory pathway in maintaining mitochondrial integrity and function, and result in accelerated disease progression. This evidence concerns the gene PRKN and Parkinson disease.