As a consequence of local inflammation, toll-like receptors (TLRs) are upregulated by lipopolysaccharide (LPS) and other microbial products and stimulate cytokine release and the activation of signaling pathways (e.g., NF-kB, JAK/STAT3, c-Jun N-terminal kinase [JNK]) that are known to fuel tumor growth [91,104]. Here, STAT3 is linked to neoplasm.