NFKB1 and digestive system neoplasm: Taken together, these data provide a molecular mechanism for n-3 PUFA-induced normalization of NF-κB DNA binding activity increased in the early phase of liver IR injury, which involves (i) nuclear NF-κBp65 sequestering through the generation of PPAR-α/NF-κBp65 complexes, and (ii) cytoplasmic NF-κB sequestering through enhanced IκB-α stability promoting its association with NF-κBp65/p50 [15].