MHC class I-restricted CD8(+) T cells are necessary to mount an immune response against Mycobacterium tuberculosis. M. tuberculosis antigens can enter MHC class I cross-processing pathways through a number of different mechanisms, including via the uptake of antigen-containing apoptotic vesicles released by infected cells. A study in this issue of the JCI by Hinchey and colleagues shows that M. tuberculosis inhibits host cell apoptosis and thus may interfere with optimal cross-priming and action of CD8(+) T cells (see the related article beginning on page 2279). M. tuberculosis genetically modified to induce apoptosis is shown to be more effective in priming CD8(+) T cells in vivo and therefore may be a more effective vaccine against tuberculosis than the currently utilized M. bovis BCG vaccine.