Other molecular factors such as transcription-coupled repair, inhibition of UNG accompanied by APOBEC3G-induced hypermutation, translesion synthesis by one of the DNA polymerases, or the role of APOBEC1 have been implicated in mutagenesis of hepatocellular carcinomas [10, 17, 69–71, 73, 74], and therefore it may be possible that the increased prevalence of APOBEC-like motif clusters in LIHC cell lines may be caused by factors other than APOBEC3B. This evidence concerns the gene APOBEC3B and hepatocellular carcinoma.