It is well recognized that various virulence factors activated by bacteria during epithelial infection are targets of NF-κB, and often recruit inflammatory cells to facilitate dissemination.40 In melioidosis infections, it is known that TNF-α and some other interleukins are involved in the early inflammatory response, and NF-κB is the key transcription factor that modulates their expression.2 These results suggest a role of the T6SS system in controlling NF-κB blockage, and it is dependent on additional factors that may be related to early infection events, such as the T3SS. Here, NFKB1 is linked to infection.