The pathobiology of MCL is complex and includes alterations in the cell cycle as a consequence of cyclin D1 over-expression driven by the chromosomal translocation t(11;14)(q13;q32) [19], abnormalities in the DNA damage response [20], and constitutive activation of key antiapoptotic pathways including phosphatidyl-inositol 3-kinase (PI3K)/Akt and nuclear factor-kB (NF-kB) [21, 22]. The gene discussed is NFKB1; the disease is mantle cell lymphoma.