research, the author found that GSTP1 promoter methylation rate was increased greatly in nonsurvived patients compared to those survived (54.71 vs. 7.08, P < 0.01). Aberrant GSTP1 promoter methylation might participate in the development and progression of ACHBLF, because the loss of GSTP1 gene expression might lead to the increase in cytotoxic molecules and liver cell damage. And the components of MELD score only reflect the consequence of liver injury. Therefore, GSTP1 promoter methylation rate might serve as a better predictive parameter for short-term mortality than MELD scores in early stage of ACHBLF. Besides all those excellent findings, there is a minor fault of that article. The author stated that 'In ACHBLF group, GSTP1 methylation level was significantly correlated with TBIL (Spearman's r = 0.29, P < 0.01), PTA (Spearman's r = À0.24, P = 0.01) and MELD score (Spearman's r = 0.26, P = 0.01)'. Although achieving values of P < 0.05, it does not indicate the strength of the Spearman rank-order correlation. In fact, an r value between 0.00 and 0.30 (or 0.00 to À0.030) usually means negligible correlation.9 Therefore, it is inaccurate to draw the conclusion that GSTP1 methylation rate is correlated with TBIL, PTA or MELD score. Nevertheless, Gao et al. have carried out meaningful work in the area of liver failure. The invalidation of GSTP1 methylation for predicting the outcome of acute-on-chronic hepatitis B liver failure or other causes of liver failure is worthy of further investigation.
ACKNOWLEDGEMENTDeclaration of personal and funding interests: None.