Aberrant stabilization and activation of HIF-1α, frequently observed in HCC patients with poor prognosis, drives tumor progression by transcriptionally activating downstream targets involved in angiogenesis (e.g., vascular endothelial growth factor [VEGF]), metabolic reprogramming (e.g., glucose transporter 1 and 3 [GLUT1 and GLUT3]), and metastasis (e.g., twist family BHLH transcription factor [TWIST]) [10–13]. This evidence concerns the gene HIF1A and neoplasm.