Although the molecular nature of the FPR-stimulating activity in sera remains to be elucidated, our further studies showed that the chemotactic activity and colony-stimulating activity contained in the supernatant of necrotic GBM cells were depleted by immunoabsorption with an antibody against annexin I (Yang et al, manuscript in preparation), suggesting that annexin I is likely a major component responsible for the FPR-stimulating activity released by necrotic GBM cells. The gene discussed is FPR1; the disease is glioblastoma.