HIF1A and neoplasm: However, the EMT to MET switch occurs slowly and often incompletely, causing tumor epithelial–mesenchymal hybrids and CSCs to persist in cervical SCC metastases: this is particularly evident in hypoxic areas where activated HIF-1 stimulates glycolysis at levels that guarantee the tumor cell hybrids and CSCs a certain independence from the vessels of the metastatic site [88,209,210,222,270,271].