Regulatory protein Tax of human T cell leukemia virus type 1 (HTLV-1) positively regulates the transcription of its own genome and specific cellular genes, and contributes to the pathogenicity in ATL, HAM/TSP and other associated diseases. The one mechanism of the transcriptional activation includes binding of Tax protein in nucleus to enhancer binding proteins of CREB, CREM, NF-kappa B p50, NF-kappa B p105 and SRF which bind to enhancer DNA. The other includes Tax-binding to NF-kappa B proteins in the cytoplasm resulting in nuclear translocation of active transcription factors. The interaction of Tax with cellular transcription factors thus ultimately results in cellular proliferation, immortalization and transformation leading to specific diseases.