As we did not find any evidence that a lack of USP28 would induce glycogen overload in DEN-induced hepatocellular carcinoma, we propose that the reduced expression of USP28 preferentially affects the reported p53/senescence pathway axis to promote tumorigenesis and cancerogenesis in CCF rather than having an additional function in regulating glycogen metabolism. Here, TP53 is linked to hepatocellular carcinoma.