As the activation of both canonical and noncanonical pathways are dependent on PRRs such as TLRs, a vital area for therapeutic interventions could be centered around the specific activation of TLRs to induce NF-κB’s protective responses against infections, such as its downstream activation of M1 and M2 macrophages, Th1 and Th17 cells, inflammasomes, and pro-inflammatory cytokines that will help aid the formation of granulomas and help to contain and decrease the bacterial load. Here, NFKB1 is linked to infection.