- Tax plays a key role in HTLV-1 pathogenicity, partly due to its capacity of constitutive NF-κB activation. Δ58Tax does not translocate to the nucleus and traps w.t. Tax molecules in the cytoplasm but still retains the cytoplasmic NF-κB activation ability. Therefore, it enhances the w.t. Tax activation of NF-κB when co-expressed at lower level than w.t. Tax. However, the double mutants Δ58Tax (M22) and Δ58Tax (148) are defective also in the cytoplasmic NF-κB activation. They were found as capable of blocking the w.t. Tax-induced NF-κB-dependent activation even when expressed at low levels. These double mutants may, therefore, be used as powerful tools for blocking w.t. Tax functions.