NBR1 and neoplasm: The increase in NBR1 binding to the ubiquitinated protein MHC‐I through the ubiquitin domain caused an increase in the degradation of MHC‐I in autophagolysosomes and a decrease in the expression of MHC‐I on the surface of tumor cells, which in turn led to tumor cell escape from CD8+ CTL immune attack (Figure9).