STAT3 and hepatitis B virus infection: Demethylation of CpGs located within octamer-binding transcription factor 4 (OCT4) and activator of transcription 3 (STAT3) cis-acting elements downstream of the SALL4 transcriptional start site TSS (SALL4TSS) enables OCT4 and STAT3 binding, recruitment of BRG1, and enhanced RNA polymerase II elongation and SALL4 transcription, inducing SALL4 re-expression in HCC associated with hepatitis B or C virus infection [143].