To further elucidate the underlying mechanisms, we examined the effects of TLR4 on the NF-κB signaling pathway and downstream pro-inflammatory cytokines, and we found that the expression of TLR4, MyD88, p-NF-κB p65, p-IκBα and p-IKKα/β and downstream pro-inflammatory cytokines TNF-α, IL-6 and IL-1β were significantly down-regulated after AT-I or shTLR4 treatment in LPS induced breast cancer cells. The gene discussed is NFKB1; the disease is breast cancer.