MDM2 and Cirrhosis: 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.