PARK7 protects against oxidative stress and maintains mitochondrial integrity, key factors in Parkinson's disease.[50] In HEK293 cells, it suppresses ferroptosis by detoxifying MGO and limiting protein glycation and lipid peroxidation.[26] In contrast, our study shows that GLO1 dysfunction—but not PARK7 deficiency—promotes ferroptosis via MGO accumulation in cancer cells, with PJA1‐mediated GLO1 degradation acting as an upstream regulatory mechanism. This evidence concerns the gene PJA1 and Parkinson disease.