During intrinsic apoptosis, mitochondrial herniation exposes the inner mitochondrial membrane (IMM) to the cytoplasm, initiating a unique form of mitophagy to deliver damaged mitochondria to lysosomes. This process occurs independently of the canonical PINK1/Parkin pathway and is driven by ubiquitination of the IMM. The study shows that IMM-induced mitophagy is a safety mechanism for cells to contain damaged mitochondria, particularly when caspase activation is incomplete or when PINK1/Parkin mitophagy is impaired. The process involves the recruitment of autophagy adaptors like P62, OPTN, and NDP52 to the IMM, which is ubiquitinated and serves as a signal for autophagosome formation. Ubiquitination of the IMM is essential for its sequestration by autophagosomes, and this process is independent of the canonical autophagy machinery. The study also reveals that IMM-induced mitophagy may play a critical role in preventing the release of mitochondrial damage-associated molecular patterns (DAMPs) during apoptosis. The findings suggest that IMM-induced mitophagy is a distinct pathway for mitochondrial clearance, which may be particularly important in situations where PINK1/Parkin-mediated mitophagy is not functional. The study highlights the importance of mitochondrial quality control in preventing inflammatory responses and maintaining cellular homeostasis.During intrinsic apoptosis, mitochondrial herniation exposes the inner mitochondrial membrane (IMM) to the cytoplasm, initiating a unique form of mitophagy to deliver damaged mitochondria to lysosomes. This process occurs independently of the canonical PINK1/Parkin pathway and is driven by ubiquitination of the IMM. The study shows that IMM-induced mitophagy is a safety mechanism for cells to contain damaged mitochondria, particularly when caspase activation is incomplete or when PINK1/Parkin mitophagy is impaired. The process involves the recruitment of autophagy adaptors like P62, OPTN, and NDP52 to the IMM, which is ubiquitinated and serves as a signal for autophagosome formation. Ubiquitination of the IMM is essential for its sequestration by autophagosomes, and this process is independent of the canonical autophagy machinery. The study also reveals that IMM-induced mitophagy may play a critical role in preventing the release of mitochondrial damage-associated molecular patterns (DAMPs) during apoptosis. The findings suggest that IMM-induced mitophagy is a distinct pathway for mitochondrial clearance, which may be particularly important in situations where PINK1/Parkin-mediated mitophagy is not functional. The study highlights the importance of mitochondrial quality control in preventing inflammatory responses and maintaining cellular homeostasis.