Purpose: To test the hypothesis that transcatheter arterial embolization (TAE) of VX2 rabbit liver tumors increases the expression of hypoxia-inducible factor-1α (HIF-1α), a transcription factor that regulates the expression of pro-angiogenic genes. Materials and Methods: VX2 tumors were implanted in the livers of eight New Zealand white rabbits. Once tumor growth was seen at T2-weighted turbo spin-echo magnetic resonance (MR) imaging, four of the eight rabbits underwent TAE with 45-150-μm polyvinyl alcohol particles. The remaining four rabbits served as non-TAE controls. The TAE end point was stasis of antegrade blood flow. All rabbits were sacrificed for tumor harvest 2 hours after TAE. Tumor tissue and corresponding normal liver tissue in each rabbit liver were stained with anti-human HIF-1α monoclonal antibody and reviewed with light microscopy. Percentages of stained viable tumor and normal liver cells were compared by using the Mann-Whitney U test (α = 0.05). Results: In eight rabbits with 24 discrete liver tumors, the mean percentage (±standard deviation) of positive HIF-1α-stained cells in the TAE group was greater than that in the control group (19% ± 7.0 vs 12% ± 8.0, respectively) (P = .05). Normal liver tissue in both the TAE and control groups showed no HIF-1α staining. Conclusion: Although HIF-1α is not expressed in normal rabbit liver parenchyma-even after TAE-HIF-1α expression is present in implanted VX2 rabbit liver tumors and significantly increased in lesions that have undergone embolization.