In 4T1 breast cancer, M1‐Exos have been shown to reprogram TAMs toward inflammatory phenotypes and stimulate proinflammatory cytokine production (e.g., IL‐6, IL‐12, iNOS).[114] More recent innovations have introduced hybrid vesicles engineered by fusing membranes from M1‐polarized macrophages and tumor cells—referred to as artificial macrophage–tumor exosomes (aMT‐Exos).[250] These chimeric vesicles exhibit improved lymph node homing and tumor site accumulation, thereby enhancing the delivery and contextualization of antigens in immunologically relevant microenvironments. The gene discussed is IL6; the disease is neoplasm.