This is in full agreement with former information showing that LPS provokes the activation of the host’s innate immune response by increasing TLR4- and MyD88-dependent signaling [47]and subsequent expression of pro-inflammatory cytokines and chemokines following binding of TLR4 [22, 47, 48], and activation of JAK/STAT signaling pathway [49] The toll-like receptor signaling pathway activates key molecules to drive immune-related responses towards infectious agents and attracts immune cells by the site of infection [29, 50]. The gene discussed is SOAT1; the disease is infection.