They exert a multifaceted plasticity adapting to different polarization states dictated by the TME M1 macrophages—“good macrophages,” induced by Th1 cytokines (e.g., IL-12, IL-18) or activated Toll-like receptors produce reactive oxygen/nitrogen species (ROS/RNS) and pro-inflammatory cytokines (e.g., IL-1β, IL-6, TNF-α) causing direct tumor cell killing. This evidence concerns the gene IL6 and neoplasm.