While the co-deletion of BCL-RAMBO and BNIP3 together may be required to reveal a role for these potential pro-apoptotic factors in modulating intracellular bacterial infections, the limited effects of pan-caspase inhibition or genetic loss of cyclophilin D or BAX and BAK, argue that abrogating mitochondrial death signaling does not significantly influence bacterial replication and infectivity. Here, BNIP3 is linked to bacterial infectious disease.