We demonstrated its capabilities by modeling the dynamics of CD4+ T cells in response to influenza infections (real and hypothetical) in different cytokine milieus, considering heterogeneous populations of Th0, Th1, Th2, Th17, and Treg subtypes and 11 cytokines in three spatial compartments (an infection site or target organ, lymphoid tissues, and a circulatory system). The gene discussed is CD4; the disease is infection.