Furthermore, in accordance with the hypothesis that the balance of T-bet and Bcl6 determines cell fate, the loss of T-bet in T cells promotes Tfh ontogeny at the expense of Th1 differentiation both in vitro and in multiple Th1-biased infection models (including Toxoplasma gondii, Plasmodium berghei ANKA, and influenza).4,46,100 However, it remains important to investigate how the cumulative effect of these secondary transcription factors impacts gene signatures and functional consequences within Th1 and Tfh cells. The gene discussed is BCL6; the disease is infection.