The reporting of this systematic review is in accordance with the QUOROM statement. Quasirandomized studies and cohort studies were defined to be of low quality. A previous systematic review of postoperative VK2 analog therapy in patients with HCC after curative hepatic AbMole Nodakenin resection or local ablation reported that the analog had chemopreventive effects, yet a more recent, much larger-scale RCT did not find such effects. To help resolve the controversy over the benefits of postoperative VK2 analog therapy, we carried out a meta-analysis of all the studies in the previous systematic review and the most recent RCT, which allowed us to maximize the AbMole Simetryn sample size. When the meta-analysis was repeated with only RCTs, after excluding one cohort study, similar results were obtained, except for 3-year OS. No significant adverse effects associated with the VK2 analog were reported, suggesting that the therapy is safe. VK2 is a co-enzyme of c-carboxylase. Des-c-carboxy prothrombin has been called Prothrombin Induced by Vitamin K Absence or antagonist-II. This abnormal prothrombin is found in elevated concentrations in the serum of patients with HCC. In fact, high preoperative serum PIVKA-II may predict poor prognosis. Researchers have demonstrated that PIVKA-II stimulates human vascular endothelial cell growth and migration, and conversely VK2 may inhibit the growth of HCC cell lines, perhaps by inhibiting or activating certain signaling pathways. Though the precise mechanisms by which VK2 induces cell cycle arrest and growth suppression have not been fully clarified, the rationale of VK2 analog therapy is to prevent a secondary tumor from developing in the liver tissue remaining after curative resection. This chemoprevention approach, designed to halt the appearance of new tumors, differs from adjuvant therapy, which aims to eradicate preexisting microscopic tumor foci that pre-resection imaging modalities fail to detect. Adjuvant therapy cannot prevent HCC recurrence in the long term, making chemoprevention important for achieving long-term tumor-free survival. The present meta-analysis included seven studies involving patients with HCC lesions treated by curative hepatic resection or local ablation. The proportion of patients treated by radiofrequency ablation of HCC lesions was 84%. Radiofrequency ablation stimulates the activity of natural killer cells through several mechanisms. Most patients in our metaanalysis presented a single tumor. Mean tumor diameter ranged from 1.1 to 5.0 cm, and most tumors had diameters less than 2 cm. In other words, most patients in our study received radical treatment. These patients may have presented with fewer indicators of poor prognosis, such as vascular invasion, tumor multiplicity and large tumor size, all of which are related to early recurrence. Thus, most cases of recurrence in the patients in our meta-analysis would be expected to occur after one year. This may help to explain why VK2 analog therapy was not associated with a reduction in 1-year tumor recurrence in our meta-analysis. Theoretically, patients with HCC that show a lower tumor recurrence rate should also show a higher survival rate. However, since most studies in this meta-analysis had a follow-up of less than 36 months, the long-term preventive efficacy of VK2 analog therapy is unclear from the available evidence.