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). The gene discussed is USP7; the disease is hepatocellular carcinoma.