BOK (BCL2 family apoptosis regulator) is a pro-apoptotic BCL-2 family member that functions primarily through the mitochondrial pathway 1. Structurally, BOK resembles the apoptotic effectors BAK and BAX 1, yet its biological functions extend beyond classical apoptosis regulation, exhibiting context-dependent roles in cell fate determination 2. Mechanistically, BOK regulates mitochondrial dynamics and neuronal calcium homeostasis 3. Notably, BOK serves as a key regulator of Parkin-mediated mitophagy by competitively binding the MCL1/Parkin complex, thereby releasing Parkin for translocation to damaged mitochondria 4. Additionally, BOK expression is required for integrated stress response (ISR) pathway activation in response to mitochondrial dysfunction 2. Disease relevance includes Alzheimer's disease, where neuron-specific BOK loss correlates with mitochondrial damage and mitophagy defects 4. BOK overexpression in hippocampal neurons ameliorates mitochondrial dysfunction and cognitive decline, while knockdown worsens disease pathology 4. BOK has also been identified as a potential biomarker and causal factor in diabetic foot ulcer pathogenesis through endoplasmic reticulum stress interactions 5. Furthermore, novel BOK-derived circular RNAs show involvement in ovarian and prostate cancer progression 6. Clinically, targeting BOK-mediated mitophagy represents a promising therapeutic strategy for Alzheimer's disease and potentially other mitochondrial dysfunction-associated diseases 4.