Glycolysis engages in chemoresistance induced by HIF-1 through different mechanisms: (1) HIF-1 switches metabolism from oxidative phosphorylation to glycolysis and leads to mitochondrial dysfunction; decreased accumulation of ROS elicits the inhibition of apoptosis, which disturbs the capability of chemotherapeutic drugs and facilitates chemoresistance (190, 193, 194); (2) Tumor-associated macrophages (TAMs) secrete vesicle-packaged HIF-1α-stabilizing IncRNA to inhibit HIF-1 degradation, promote glycolysis, and induce docetaxel resistance in breast cancer. The gene discussed is HIF1A; the disease is neoplasm.