FDG PET imaging has been applied for about a decade. It is generally accepted that imaging the metabolic activity of tumor tissue provides more sensitive and more specific information about the extent of disease than morphologic or anatomic imaging alone. The metabolic activity offers additional information about cancer biology and can be used to determine tumor aggressiveness and also help to assess response to treatment (1, 2). In contrast, the rate-limiting step for the cellular accumulation of 18F-FDG in different tissues is still not fully understood. The uptake mechanism and biochemical pathway of 18F-FDG has been extensively studied in vitro and in vivo, and the transport through the cell membrane via glucose transport proteins (GLUTs) and the intracellular phosphorylation by hexokinase (HK) have been identified as key steps for subsequent tissue accumulation. As FDG-6-phosphate is not a suitable substrate for glucose-6-phosphate isomerase, and the enzyme level of glucose-6-phosphatase is generally low in tumors, FDG-6-phosphate accumulates in cells and is visualized by PET. 18F-FDG uptake in tissue, however, is not tumor specific and little is known about the underlying cellular mechanisms of 18F-FDG accumulation in inflammatory tissue. Therefore, the study by Chung et al. on pages 999–1003 in this issue of The Journal of Nuclear