Taking advantage of the specific Tfr sensitivity to interleukin-2 (IL-2), Botta et al. first used rIL-2-treatment to deplete Tfr cells in influenza-infected mice and observed that the frequency of anti-histone IgG antibody-secreting cells (ASCs) increased in treated mice, suggesting that a lack of Tfr cells results in the development of anti-nuclear antibody responses. The gene discussed is IL2; the disease is influenza.