By profiling the apoptotic response of phagocytes along with the exploration of the allelic repertoire of human CASP9, we show that staphylococcal death-effector deoxyribonucleosides and coupled alterations in intracellular nucleotide pools provoke mitochondrial damage and subsequent ignition of the intrinsic pathway of apoptosis, an immunological silent event that helps S. aureus to establish abscesses in host tissues. The gene discussed is CASP9; the disease is abscess.