ATLL is believed to originate from regulatory T cells (Tregs) based on the Treg phenotype, for example, expression of CD4, CD25, CD127, and Foxp3, as observed in our case.[5] In the present case, investigation of the immunoregulatory receptors on CD4+ ATLL cells showed that they express PD-1, ICOS, and CXCR3; partially express CCR6 and CXCR5; and lack CTLA4 and TIM3. The gene discussed is HAVCR2; the disease is adult T-cell leukemia/lymphoma.