These results confirm that LXR activation exerts a similar effect on macrophages generated in the presence of either M-CSF or tumor-derived ascitic fluids, and demonstrate that LXR activation opposes the polarizing action of pathological tumor-derived fluids by impairing the acquisition of the genes that characterize anti-inflammatory (M-CSF-dependent) macrophages and enhancing the expression of genes that define pro-inflammatory macrophages. This evidence concerns the gene CSF1 and neoplasm.