“…To our knowledge, there is not yet a review that summarizes the results of basic and clinical studies that investigate the role of endoglin in HCC progression. Hence, an attempt to fill this gap was made in this manuscript, choosing endoglin as its focus for several reasons: (1) expression of that glycoprotein represents the proliferation status of liver sinusoidal ECs (LSECs), which are key in angiogenesis of the HCC microenvironment; (2) endoglin seems to be a better quantitative marker of microvessels density (MVD) compared to other microvessel markers e.g., CD34 [15], which allows for more credible evaluation of HCC angiogenesis in humans; (3) the results of studies on the role of endoglin in pathogenesis and clinical treatment of HCC are not coherent, with the causes of that divergence currently unexplained [14,15,16,17,18,19,20,21,22]; (4) there is currently no meta-analysis of the diagnostic-prognostic role of that marker in HCC; (5) while endoglin is a promising target of anti-angiogenic therapy of solid tumours, there are not many clinical trials of its application in advanced HCC [10]; and (6) comparison of the available results of studies on the role of endoglin in HCC, as well as the function of that glycoprotein in liver physiology, seems to be of great practical (diagnostics, prognostics, therapy) and basic scientific importance.…”