Although studies have shown that the HGF/c-Met pathway is abnormally activated in cancer and can promote tumor proliferation, invasion, metastasis, and angiogenesis by stimulating the PI3K/AKT, Ras/MAPK, JAK/STAT, SRC, Wnt/β-catenin, and other signaling pathways (10, 34), our study suggested that HGF/c-Met signaling may inhibit the development of tumor cells transformed from normal cells with high expression of HGF through the regulation of these two pathways, and thus provides a direction for the mechanism of our future research. Here, MET is linked to neoplasm.