The results revealed that several canonical signaling pathways were significantly enriched, some of which have already been shown to be involved in the inflammatory response (e.g., cytokine-cytokine receptor interaction, NOD-like receptor signaling pathway, Toll-like receptor signaling pathway, NF-κB signaling pathway, chemokine signaling pathway, IL-17 signaling pathway, Staphylococcus aureus infection, and TNF signaling pathway), and pathogenic microbial infection (e.g., influenza A, herpes simplex infection, TNF signaling pathway, and human T cell leukemia virus 1 infection) (Fig. 3B). This evidence concerns the gene TNF and staphylococcus aureus infection.