In CRC, LPS-TLR4/myeloid differentiation protein 2 (MD2) signaling paradoxically stimulates PI3K/AKT/β1 integrin pro-metastatic pathways (245)—a contrast to its role in osteosarcoma, where LPS-TLR4 activation increases CD8+ T cell infiltration into lung metastases to suppress tumor progression (220, 221), and in radiotherapy, where LPS enhances anti-tumor immunity via TLR4 by boosting dendritic cell activation and effector T cell recruitment (221). The gene discussed is AKT1; the disease is neoplasm.