Correlative assays showed sustained production of IFNγ by NK cells only in those pts experiencing a clinical response or stabilization of disease. Elevated serum levels of MIP-1, TNF-α, and the antiangiogenic factors IP-10 and MIG were also observed in these pts. Pts genotyping suggested that a specific IFN-γ gene polymorphism might have been associated with increased IFN-γ production. The ability of pts PBMC to conduct ADCC against tumor targets in vitro did not correlate with clinical response or dose of IL-12. This evidence concerns the gene CXCL9 and neoplasm.