STING1 and neoplasm: Mechanically, we elucidated a novel direct pathway whereby MNC-168 activities the STING-IFN-I pathway through the secretion of bacterial membrane vesicles (MVs) to target the tumor and enhance antitumor immunity, which distinguished from previous reports on bacterial CDNs in STING activation,21 flagellin of Enterococcus gallinarum MRx0518 in TLR5 activation.56 and SagA of Enterococcus in NOD2 activation.18 Furthermore, we validated the augmenting effect of MNC-168 on anti-PD-1 therapy across multiple preclinical cancer models, reinforcing its translational potential.