Our findings in the NHP model of HIV infection support the notion that cells harboring intact proviruses are particularly dependent on BCL-2 for survival, as evidenced by the fact that venetoclax treatment resulted not only in an overall reduction in CD4+ T-cell counts but in a specific decline in the frequency of BCL-2+ cells and CD4+ T-cells containing intact proviruses. The gene discussed is BCL2; the disease is HIV infectious disease.