In line with the widely accepted role of NF-κB as the downstream mediator of Tax to drive tumorigenesis, genetic deletion of NF-κB2 significantly prevents the tumorigenesis/neurofibromas in Tax transgenic (Tax+) mice in which Tax expression is driven by the HTLV-I Long Terminal Repeat (LTR) promoter [28]. The gene discussed is CNTN2; the disease is neurofibroma.