M1 macrophage-derived exosomes were transfected with NF-κB p50 siRNA and miR-511-3p to foster M1 polarization and subjected to surface modification with the IL4R-targeting IL4RPep-1 peptide (CRKRLDRNC) using a phospholipid anchor; these constructs inhibited tumor progression by reprogramming IL4R-high and M2-polarized TAMs to an M1-like phenotype39. The gene discussed is IL4R; the disease is neoplasm.