Su et al. (2007) compared the promoter methylation in p14 (ARF), p16 (INK4a), O(6)-methylguanine-DNA methyltransferase (MGMT), glutathione S-transferase pi (GSTP1), and E-cadherin (E-Cad, also CDH1) in noncirrhotic, cirrhotic, and HCC tissues; p16(INK4a) promoter methylation increased along with liver disease progression; GSTP1 promoter hypermethylation occurred more frequently in HBV related HCC; while p16(INK4a), MGMT, and p14(ARF) promoter hypermethylation did not show this tendency [22]. This evidence concerns the gene CDKN2A and liver disorder.