Several studies have demonstrated that the expression of BCR-ABL kinase activity in CML cell lines leads to a constitutive activation of NFκB through IKKβ downstream of BCR-ABL and the suppression of NFκB activation by the expression of IκBα blocked BCR-ABL-dependent xenograft tumor formation [161–163]. The gene discussed is ABL1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.