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. This evidence concerns the gene NOS2 and neoplasm.