Given the role of MAPKs in the host response to F. tularensis (33, -, 37), we examined if infection of murine bone marrow-derived macrophages (BMMs) with the LVS ΔtolC mutant leads to increased p38, SAPK/JNK, or ERK1/2 activation in comparison to infection with the WT LVS. The gene discussed is MAPK9; the disease is infection.