Tumor growth was reduced after peritoneal macrophage depletion by administration of clodronate‐loaded liposomes, or Irg‐1 silencing in peritoneal macrophages by lentiviral shRNA leading to decreased ROS production, supporting that LPMs had a tumor‐promoting function.[86] Interestingly, in this experimental setting, the protumor phenotype of LPMs was not related to the expression of prototypical protumor genes, such as IL10, TGFB, and Retnla, but proinflammatory genes, such as IL6, TNFA, and IL1B. The gene discussed is IL6; the disease is neoplasm.