NFKB1 and cancer: In fact, in the classical pathway, NF-κB can be maintained inactive within the cytoplasm through interactions and binding to inhibitor of κB (i-κB) in normal cells, whereas it is constitutively activated in cancer cells; the phosphorylation of i-κB protein results in it being targeted by protease, releasing NF-κB that is translocated to the nucleus where it acts as transcription factor, leading to the expression of genes related to apoptosis, cell cycle control, adhesion, and migration [89].