Expansion of these T-cells results from the expression of the viral oncoprotein Tax-1, which in turn activates transcription factors (e.g. cAMP-dependent transcription factor, nuclear factor kappa-B [NF-κB]), inhibits apoptosis (e.g. repression of p53), disrupts cell cycle control, and interferes with genetic stability (DNA polymerase β, proliferating cell nuclear antigen, and the mitotic spindle-assembly checkpoint protein MAD1) .6–10 It is still unclear why only 2–5% of patients infected with HTLV-1 develop ATLL. Here, NFKB1 is linked to adult T-cell leukemia/lymphoma.