Taken together, these molecular and cytological assays showed that DNAAF5 recruits USP39 and PFKL by acting as a scaffold protein, and enhances PFKL protein stability in the form of deubiquitination through interactions between USP39 and PFKL, which accelerates glycolysis to promote the malignant processes of HCC. The gene discussed is PFKL; the disease is hepatocellular carcinoma.