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. The gene discussed is PINK1; the disease is Parkinson disease.