BNip3 channel-forming protein (Bocharov et al., 2007). It is an apoptosis-inducing protein that can overcome BCL2 suppression and may play a role in repartitioning calcium between the two major intracellular calcium stores in association with BCL2 (Ghavami et al. 2010). It is also involved in mitochondrial quality control via its interaction with SPATA18/MIEAP: in response to mitochondrial damage, it participates in mitochondrial protein catabolic process (also named MALM) leading to the degradation of damaged proteins inside mitochondria. The physical interaction of SPATA18/MIEAP, BNIP3 and BNIP3L/NIX at the mitochondrial outer membrane regulates the opening of a pore in the mitochondrial double membrane in order to mediate the translocation of lysosomal proteins from the cytoplasm to the mitochondrial matrix (Nakamura et al. 2012). Platinum-based combination chemotherapy triggers cancer cell death through induction of BNIP3 and ROS, but not autophagy (Chung et al. 2020).