Moreover, it is plausible that up-regulation of TLRs and activation of inflammatory signaling and production of cytokines by CSE contributes to disease pathogenesis and provides the basis for the use of inhibitors of TLR2, TLR3, ERK1/2 and NF-κB to diminish CS-induced human hematoxic effects as a preventative measure against cancer for long term smokers and their families. The gene discussed is TLR2; the disease is cancer.