Mechanistically, SLITRK4 mediated CRC metastatic growth through several mechanisms,[1] regulating PI3K/AKT signaling pathway in cell proliferation and survival,[2] promoting tumor angiogenesis by upregulating VEGFA,[3] regulating extracellular matrix and cell‐matrix adhesion molecules, and[4] enhancing TAM infiltration and polarization, releasing tumor growth‐promoting factors and cytokines and further inducing immune tolerance. This evidence concerns the gene AKT1 and neoplasm.