Since tumor hypoxia plays a critical role in deciding the phenotype of TAMs and further assisting neoangiogenesis [53,54], our results implied that KDELC2 might induce tumor vascularization via the initial enhancement of HIF-1α expression, and hypoxic TME production induced ROS promotion, ER stress activation, and M2 TAM proliferation. The gene discussed is HIF1A; the disease is neoplasm.