HIF1A and neoplasm: For example, some of the anticancer agents are proteasome inhibitors (bortezomib and nelfinavir) that utilize the UPR pathways to decrease VEGF levels and thus directly inhibit tumor vasculature [299–302], whereas the ER chaperones inhibitor 17-AAG (geldanamycin) reduces the degree of adaptive HIF-1 signaling and thus stimulates hypoxic cell death [303, 304].