The enhanced AKT phosphorylation can be blocked by eritoran (a TLR4 antagonist), PI 103 [a phosphatidylinositide 3-kinases (PI3K) inhibitor], or anti-β1 integrin antibodies that are known to ameliorate CRC and its metastatic behavior (75–77), indicating that the PI3K/AKT signaling pathway is induced by TLR4 in response to LPS binding and plays a central role in the growth and progression of CRC. The gene discussed is AKT1; the disease is colorectal carcinoma.