Since HBV infection is a well-established risk factor for the development of HCC, HBV infection status in control population could be the source of bias and may explain the instability of the comparison between genotype CC and GG. However, stratified analysis by HBV status in controls showed consistent results suggesting no significant difference of susceptibility to HCC existed between CC and GG genotypes, which suggested HBV status may not be the main factor that influenced the stability of this comparison. However, lack of detailed information of both cases and controls prevented us from further exploring the potential source of the inconsistency observed in sensitivity analysis. In conclusion, possible association between rs2910164 polymorphism and HCC risk should not be ruled out and this result should be interpreted cautiously. Another SNP shown to have potential relationship to the risk for HCC is ABT-199 Bcl-2 inhibitor rs11614913 in miR-196a2. It is reported that C allele of rs11614913 increased the expression of mature miR-196a2 in HCC tissues. Of note, several genes involved in carcinogenesis including homeobox and annexin A1 have been reported to be the target of miR-196a2. HOX genes encode important transcription factors during normal development and in carcinogenesis. The disorder of HOX proteins was suggested to play a crucial role in hepatocarcinogenesis and the progression of HCC. Acting as a mediator of apoptosis and inhibitor of cell proliferation, ANXA1 participates in various physiological and pathological processes. Masaki et al. demonstrated that ANXA1 participated in the malignant transformation of HCC and was closely related to the malignant behavior of HCC. Therefore, alterations in miR-196a2 may contribute to susceptibility to HCC through the deregulation of target genes including HOX and ANXA1. Indeed, recent studies have reported the association of miR-196a2 rs11614913 polymorphism with HCC risk. However, in another study, no association between rs11614913 and HCC was observed. 4 studies on the relationship between rs11614913 and susceptibility to HCC were included in our meta-analysis. To our surprise, we failed to find any association between rs11614913 polymorphism and the risk for HCC in any of the examined genetic models. Similarly, subgroup analysis in Chinese population also showed no association of miR-196a2 rs11614913 polymorphism with susceptibility to HCC. Sensitivity analysis found no significant influence of any single study on pooled ORs, indicating the stability of this meta-analysis was acceptable. To the best of our knowledge, this is the first meta-analysis evaluating the potential association between two common polymorphisms rs2910164 in miR-146a and rs11614913 in miR196a2 and susceptibility to hepatocellular carcinoma. However, caution should be made when interpreting the results due to some limitations of this meta-analysis. Firstly, heterogeneity was detected in some comparisons of rs11614913 and sensitivity analysis showed that the study from Zhang et al. had a significant influence on the evaluation of potential association.