They found that the AIEgen (tTDCR) mediated type I mechanism was the main driver for M1‐polarization.[110] Mechanistically, the generated ROS activated NF‐κB signaling pathway through promoting phosphorylation and nuclear translocation NF‐κB, which down‐regulated M2‐related makers and up‐regulated M1‐related makers, leading to great ablation of 4T1 tumor. The gene discussed is NFKB1; the disease is neoplasm.