PTX3 deficient tumors showed enhanced complement C3 deposition and C5a levels, CCL2 production, and tumor-promoting macrophage recruitment, which was attributed to dysregulated complement activation since C3-genetic inactivation and CCL2 inhibition reverted the phenotype and the increased susceptibility to mesenchymal carcinogenesis in PTX3-deficient mice. The gene discussed is PTX3; the disease is neoplasm.