Human T cell leukemia virus type I (HTLV-I) is the causative agent of a fatal malignancy known as adult T cell leukemia (ATL). The HTLV-I Tax protein is thought to play a significant role in the initiation and pathogenesis of HTLV-I-mediated disease. Tax is a potent oncogene that deregulates cellular gene expression by persistently activating signaling pathways such as NF-kappaB. Tax activation of NF-kappaB is critical for the immortalization and survival of HTLV-I-infected T cells. In this review, we describe recent insights into the mechanisms employed by Tax to activate the canonical and noncanonical NF-kappaB signaling pathways. The adaptor function of Tax appears to be a common and important mechanism for the pathological activation of both NF-kappaB pathways.