SOCS1 silencing by CpG island hypermethylation in HCC has been demonstrated in several previous studies.3, 23 In addition, due to SOCS1’s role as a negative JAK/STAT pathway regulator, it may also be an HCC tumor suppressor.23 Our findings indicated that miR-29a suppressed SOCS1 mRNA expression by directly targeting TET enzymes, leading to SOCS1 promoter hypermethylation, SOCS1 suppression and STAT3 signaling activation. Here, STAT3 is linked to neoplasm.