As Endostatin has been shown to downregulate HIF-1α, we, therefore, propose that the synergistic effects of pHGFK1 and pEndo+pHGFK1 on CSCs in the tumor environment may be at least partly attributed to the combined effects of the receptor antagonistic function of HGFK1 on the HGF/SF-Met pathway and the inhibition of HIF-1α induced by the overexpression of Endostatin. The gene discussed is HIF1A; the disease is neoplasm.