From a mechanistic perspective, DNAAF5 directly binds to PFKL (a key rate-limiting enzyme in glucose metabolism) and recruits USP39, which deubiquitinates PFKL to enhance the stability of the PFKL protein, thereby enhancing aberrant glycolysis and accelerating the malignant progression of HCC in HCC cells. The gene discussed is PFKL; the disease is hepatocellular carcinoma.