Thus, the increased levels of proliferation of CD4+ and CD8+ T cells in HIV-1 infection are not primarily related to a homeostatic mechanism to compensate for loss of CD4+ T cells directly killed by HIV-1, but rather are due to extensive and chronic viral-induced immune cell activation followed by bystander CD4+ and CD8+ T cell apoptosis (13)—a fundamental aspect of the associated immunodeficiency. The gene discussed is CD8A; the disease is HIV-1 infection.