Kim et al. showed that Lewis lung carcinoma (LLC) was the most powerful macrophage activator leading to production of interleukin-6 and tumor-necrosis factor-α through activation of the Toll-like receptor (TLR) family members TLR2 and TLR6 [9] and their results explained how advanced cancer cells change the host innate immune system and thus generate an inflammatory microenvironment. The gene discussed is TLR2; the disease is Carcinoma, Lewis Lung.