These observations are attributed to TRIM21’s dual effector and sensor roles, as it not only mediates ADIN but also initiates an innate immune response upon infection with antibody-coated pathogens by recruiting the proteasomal system for degradation and simultaneously activate transcription factors (NF-κB/IRFs/AP-1) resulting in a proinflammatory response (27, 28, 75). The gene discussed is NFKB1; the disease is infection.