To this end, we recently described a convenient and relevant model system [6] in which resting peripheral blood CD4 T cells are treated with common gamma chain cytokines such as IL-4 that render them permissive to infection without inducing cell activation, though it is known that common gamma chain cytokines induce signaling pathways such as stat5 or stat6 and increase the expression of the survival protein Bcl-2 [31, 32]. The gene discussed is CD4; the disease is infection.