Like eukaryotes, bacteria possess a variety of mechanisms, such as NAD+ depletion, to counteract viral infections but many details of phage defense are currently not understood. We recently uncovered the unusual mechanism which controls activity of the bacterial virulence factor and phospholipase PlaB by NAD+. Specifically, physiological concentrations of NAD+ stabilize inactive PlaB tetramers while low NAD+ results in dissociation into active PlaB dimers and unleashment of fierce phospholipase activity. Since NAD+ is usually confined to the intracellular milieu, we presumed an intrinsic function of PlaB in programmed bacterial cell death which is key to abortive phage infection (abi). Now we aim to analyze PlaBs characteristics as a putative death effector and its interplay with NAD+ depletion in the context of phage infection.