TEP1 and infection: Given that the depletion of TEP1-F and SPCLIP1, and the cleavage of CLIPA8 were comparable in the two infection models, another possibility is enhanced lethality is driven by a distinct response due to a feature distinct to S. aureus. This possibility is supported by the differential effect we find regarding APL1C cleavage as well as previously observed differences in genes required for phagocytosis [16].