Overexpression of MUL1 compensates for PINK1 or Parkin loss in PD, rescuing the PINK1 and parkin mutant-induced phenotypes in dopaminergic neurons and muscles, indicating that MUL1 acts in parallel to the PINK1-Parkin pathway.89 Notably, MUL1 acts upstream of PINK1 and promotes PINK1 stability, inducing mitophagy independently of mitochondrial depolarization.90 In addition, MUL1 conjugation to UBE2E3 (ubiquitin-conjugating enzyme E2 E3) can bind GABARAP, but not LC3 (Fig. 4b).91 These observations indicate that MUL1 functions as both a ubiquitin ligase and a mitophagy receptor. The gene discussed is PINK1; the disease is Parkinson disease.