HIF1A and hepatocellular carcinoma: The results of assays suggested that the amino‐terminal two‐thirds (amino acids 1‐570) of PROX1 was responsible for the interaction with HIF‐1α, upregulating HIF‐1α expression to induce EMT response in HCC cells.21 Another research had showed that PROX1 could prevent p65 ubiquitination by recruiting USP7 to inhibit HCC angiogenesis.19 Therefore, we focused on the ubiquitination of HIF‐1α that a reversible process is dependent on deubiquitylating enzymes (DUBs).