To be specific, when TLR4 is activated, MyD88 is urged to recruit the TIR domain of TLR4; then, the degradation of IκBα and the activation of NF-κB are induced; the transcription of proinflammatory factor genes such as TNF-α, IL-6, and IL-1β is enhanced; and the synthesis and release of TNF-α, L-6, and IL-1β are correspondingly increased; then the increase in the contents of TNF-α, IL-6, and IL-1β further strengthens the activation of NF-κB, promotes the nuclear transfer of NF-κB, and then aggravates immune inflammation [28]. The gene discussed is NFKBIA; the disease is inflammation.