In addition to the inherent potential against vessel‐targeting agents, including high pericyte coverage of vessels, acquired drug resistance, such as over‐expression of alternative signaling pathways, is recognized as an important mechanism of tumor evasion from angiogenic suppression.43, 44 In this study, whereas the expression of VEGFR2, a major target of sorafenib, diminished in both the tumor center and periphery, the activities of CD31 (vessel formation) and Ki67 (cell proliferation) were preserved in the tumor periphery. This evidence concerns the gene MKI67 and neoplasm.