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In 1969, Edwards and Hayes (1) noted that gal lium-67 accumulated in involved lymph nodes in Hodgkin's disease. Since then, Ga-67 has been shown to localize in a variety of tumors as well as inflammatory lesions. Some studies (2,3) have suggested that Ga-67 uptake by inflammatory lesions is due mainly to its concentration by polymorphonuclear leukocytes (PMN) at the sites of inflammation. However, in vitro studies ofGa-67 uptake have consistently revealed that PMNs do not significantlyaccumulateGa-67unlessthe plasma membrane's permeability barrier is disrupted (4—6). Gallium-67 is also taken up by a variety of micro organisms (7), but analysis of abscess contents reveals that most of the Ga-67 is in the noncellular fraction (2,500 g supernate) (4,8). Furthermore, Ga-67 accu mulates in inflammatory lesions of agranulocytic ani mals (8) and patients (9), in whom no PMNs are found in the circulation or at the sites of infection. Thus, neithe