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We read with great interest the letter by Sheng and Shui. The data presented are consistent with our initial observation that the cluster of differentiation (CD)24 polymorphism associates with progression from chronic hepatitis B Virus infection to liver cirrhosis and hepatocellular carcinoma (HCC).1 We also reported, in a transgenic model of HCC, that targeted mutation of the CD24 gene reduces the size of HCC in the mice. The compelling data by Sheng and Shui raised an import issue on the role for CD24 in HCC pathogenesis. Although we have not observed CD24 expression in HCC samples, recent work by Lee et al.2 suggests that CD24 is a marker for HCC stem cells and may play an important role in HCC stem cell function. It would be of great interest to determine whether the function of CD24 is to regulate adaptive3 and innate immune responses4 or HCC stem cell function2 or both.

Yang Liu Ph.D.*, Shengdian Wang M.D., Ph.D.†, Fusheng Wang M.D., Ph.D.‡, Dongling Li M.D.†, Linghua Zheng Ph.D.†, Pan Zheng M.D., Ph.D.*, * Departments of Surgery, Pathology, and Internal Medicine, University of Michigan, Ann Arbor, MI, † Institute of Biophysics, Chinese Academy of Science, Beijing, China, ‡ PLA Hospital No. 301, Beijing, China.

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