And in the hypoxic tumor microenvironment of HCC, CFL1 can be transcriptionally activated by hypoxia-inducible factor-1α (HIF-1α), and subsequently interacts with PLD1 to inhibit PLD1 ubiquitination degradation and stabilize its expression, thereby activating the AKT pathway [24]. The gene discussed is HIF1A; the disease is neoplasm.