Viruses mercilessly exploit their host cells to guarantee their own proliferation and propagation. To achieve this goal, many viruses suppress the apoptotic program, thereby avoiding premature death of the host cell. Indeed, apoptosis of infected cells may be considered as a pristine defense against infectious pathogens, as illustrated by a simple Gedankenexperiment: if all host cells died immediately after infection, then the virus could not replicate. It is only at late stages of the viral life cycle that some viruses actively induce apoptosis, either in their host cells or, via a variety of different strategies, in immunologically relevant cells, with the specific aim to subvert the host’s innate or cognate immune response. As viruses have coevoluted with their host to adapt to particular ecological niches, they have “learned” to target strategic processes in their host cell’s biology. One fascinating example is now provided by the poxvirus that causes myxomatosis, a lethal disease which has been eradicating entire populations of rabbits. Myxoma virus codes for a protein designated M11L, which, as shown in this issue (1), inhibits host cell apoptosis by acting on the peripheral-type benzodiazepine receptor (PBR).