In agreement, we detected a strong activation of classical apoptotic initiator (caspases-9, -8) and effector (caspases-3, -7) caspases as well as phosphorylation of apoptosis-related kinases p38 MAPK and JNK in caspase-1/11-deficient macrophages after infection with B. pseudomallei (Figure 3) indicating that in the absence of caspase-1/11, alternate cell death pathways such as apoptosis might compensate for the lack of pyroptosis. Here, CASP3 is linked to infection.