reported that the autophagy transport receptor NBR1 binds to MHC‐I through the ubiquitin‐binding domain, mediates the degradation of MHC‐I molecules in autophagolysosomes, and promotes immune escape in patients with pancreatic cancer.[16] According to our study, we found that M2‐TAM exosomes, derived from LINC01232, promote tumor immune escape through the E2F2/NBR1/MHC‐I axis. This evidence concerns the gene NBR1 and familial pancreatic carcinoma.