Bnip3l induces apoptosis. It interacts with viral and cellular anti-apoptosis proteins. It can overcome the suppressors BCL-2 and BCL-XL, although high levels of BCL-XL expression will inhibit apoptosis. It inhibits apoptosis induced by BNIP3. It is involved in mitochondrial quality control via its interaction with SPATA18/MIEAP: in response to mitochondrial damage, participates to mitochondrial protein catabolic process (also named MALM) leading to the degradation of damaged proteins inside mitochondria. Bnip3l may function as a tumor suppressor.