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We read with great interest the publication by Dhar et al.1 and congratulate the authors. We agree that the measurement of serum endostatin can predict tumor vascularity and may serve as a promising tool in antiangiogenic therapy for patients with HCC.

At the same time, the 184-amino acid proteolytic fragment of the carboxy terminus of C18, endostatin, has been identified as a potent endogenous inhibitor of angiogenesis. The liver is the main source of endostatin in humans and mice. Hepatocytes are a major source of C18 expression in liver.2 Therefore, liver resection (especially major hepatic resection) may alter postoperative endostatin levels but to our knowledge there are no data published to date in the literature regarding this matter.

We conclude that endogeneous endostatin release must be considered after liver resection.

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