In addition, it was found that the repeated mutations of CTNNB1 and the activation of the NFE2L2/kelch-like ECH-associated protein 1 pathway played an important role in the occurrence of HB, which confirmed the stability loss of the genome and the deletions of the telomerase reverse transcriptase promoter as prominent characteristics of aggressive HB with HCC features (12). This evidence concerns the gene KEAP1 and hepatocellular carcinoma.