Using the resistant C57BL/6 mice model chronically infected with L. major, Peters et al. demonstrated that a short-lived subset of IFN-γ-producing effector T cells (CD44+CD62L-T-bet+Ly6C+), which require continuous exposure to antigens and are not derived from reactivated memory cells, mediate Th1 concomitant immune response to a secondary infection [178]. The gene discussed is IFNG; the disease is infection.