In addition, Pengbo Cao et al.54 also found a possible mechanism of HBV-related HCC development without cirrhosis because of MDM2–p53 axis dysfunctions; the expression of small nucleolar RNAH/ACA box 18-like 5 (SNORA18L5) in hepatocytes can be upregulated by HBV, which promotes p53 ubiquitination and degradation by preventing RPL5 and RPL11 (ribosomal proteins) to escape into the nucleoplasm to bind MDM2. Here, TP53 is linked to hepatocellular carcinoma.