It could also cause reactive oxygen species, followed by the activation of TLR4/NF-κB pathway, which could promote the production of pro-inflammation factors (TNF-α, IL-1β, and IL-6), and accelerate apoptosis (Bax/Bcl-2), and ultimately aggravated tissue damage and lead to bacterial, viral, and fungal infections (38, 39). This evidence concerns the gene TNF and fungal infectious disease.