These results suggested that during the clonal evolution of metastatic LUAD, the IGF2BP2-overexpressing LUAD cell subpopulation diffuses IGF2BP2 into the tumor microenvironment and is taken up by endothelial cells by cellular internalization, which subsequently targets to enhance the RNA stability of FLT4 through m6A modification, thereby activating the PI3K-Akt signaling pathway, and promoting angiogenesis (Fig. 6M). The gene discussed is AKT1; the disease is neoplasm.