The role of MK2 and MK3 in LPS-induced inflammatory signaling is well-established in vivo; MK2 knockout mice show increased resistance to endotoxic shock and increased susceptibility to infections (Kotlyarov et al., 1999; Lehner et al., 2002) and this phenotype is exacerbated by simultaneous deletion of MK3 (Ronkina et al., 2007). This evidence concerns the gene MAPKAPK3 and infection.