During signal transduction, TLR activates nuclear factor κ-beta (NFκB) [133], the main pro-inflammatory promoter prevailing in the tumour microenvironment, leading to increases in pro-inflammatory cytokines such as TNF-α, IL-1β, and IFN-γ but reductions in anti-inflammatory molecules such as interleukin 10 (IL-10), SOD, CAT, and GPx (Figure 1(a)). The gene discussed is NFKB1; the disease is neoplasm.