NFKB1 and neoplasm: Conversely, ingeniously engineered bacterial outer membrane vesicle-based nanoplatforms (OMV@NP) actively induce M1 polarization through the TLR4/MyD88/NF-κB pathway activation, and when strategically combined with antigen and adjuvant release systems, effectively reverse tumor-induced immunosuppression by reprogramming the myeloid compartment (149).