It was found in the present experiments that conditional knockout of the SHP-2 gene and removal of the dephosphorylation activity of SHP-2 could contribute to the activation of the Ang/Tie2-PI3K/Akt/mTOR pathway in TEMs, thus strengthening the tumor micro angiogenesis in the TME and facilitating CRC liver metastasis. The gene discussed is AKT1; the disease is neoplasm.