The cellular and molecular processes through which HTLV-1 leads to the development of ATLL are complex, as they involve a series of mechanisms such as genomic integration, epigenetic reprogramming, persistent clonal expansion, and RNA-based modifications and alternative splicing, processes in which various proteins, including Tax and HBZ, play a role. The gene discussed is HBZ; the disease is adult T-cell leukemia/lymphoma.