During infection, a cascade of signals leads to the recruitment of inflammatory cells (neutrophils and macrophages), which phagocytose damaged cells and infectious agents, thus promoting the secretion of pro-inflammatory cytokines and chemokines (e.g., tumor necrosis factor (TNF) and interleukin 1 (IL-1)) for the subsequent activation of adaptive immune responses [17,18]. This evidence concerns the gene TNF and infection.