Given the potent anti-inflammatory effects of PPARγ by transrepression of NF-kB and stabilization of co-repressor complexes on promoters of pro-inflammatory genes [1], such induction of PPARγ in macrophages upon bacterial infection may give rise to escape from innate immune responses acting on various immune effector mechanisms, because PPARγ targets many pro-inflammatory genes [8]. Here, NFKB1 is linked to bacterial infectious disease.