Remarkably, our results derived from KML001-treated CD4 T cells are similar to the findings in T cells during chronic viral (HCV, HIV) infection in that these CD4 T cells show a senescent status, characterized by telomere erosion due to TRF2 inhibition via the p53- and Sirt6-mediated ubiquitin degradation, and are more vulnerable to telomere loss-mediated cell apoptosis. The gene discussed is TERF2; the disease is HIV infectious disease.