The TLR4 signaling pathway can be specifically triggered by lipopolysaccharide (LPS) (7), an endotoxin from the Gram-negative bacteria, resulting in myeloid differentiation primary response protein 88 (MyD88) dependent or MyD88-independent pathway activity that releases downstream pro-inflammatory cytokines, such as interleukin (IL)-1β and tumor necrosis factor (TNF)-α, to eliminate infection (8). This evidence concerns the gene MYD88 and infection.