NFKB are transcription factors. NFKB1 is in human chromosome 4q23 and NFKB2 in human chromosome 10q24. The former codes for a protein p105 and the latter for p49. Both are regulators of viral and cellular genes. IKKβ is essential for IκB phosphorylation and its subsequent degradation, leading to the activation of NFKB1. IKKα seems to be involved in the activation of NFKB2 through phosphorylation of histone H3 (Anest V et al 2003 Nature [Lond] 423:659). They also have homology to the REL retroviral oncogene and the product of the Drosophila maternal gene dl and some regulatory proteins of plants. NF-κB is selectively activated by the nerve growth factor using the neurotrophin p75 receptor (p75^NTR), a member of the tyrosine kinase family, located in the Schwann cells. NF-κB usually exists within the cell, in association with the inhibitory molecule IκB. Their dissociation (induced by TNF, IL-1, etc.) permits NF-κB to move into the nucleus. NF-κB regulates the expression of cytokine genes, acquired immunodeficiency, cancer metastasis, rheumatoid arthritis, inflammation, and other processes. Protein kinase Θ mediates NF-κB activation via a T cell receptor and CD28.  oncogenes,  cancer,  angiogenesis,  morphogenesis in Drosophila {3},  Schwann cell,  AKT,  IκB,  IKK,  NF-κB; Senftleben U et al 2001 Science 293:1495; Claudio E et al 2002 Nature Immunol 3:958.