In contrast, during influenza infection, there is likely a competing cytokine, such as IL-6, that may allow the Tfh fate to be promoted, even when IL-2 consumers are lacking in the absence of T-bet.46 Consistent with this, recent research led by the Ballesteros group found that GC Tfh cells utilized cell-intrinsic IL-6 signaling, which blocked STAT5 from binding to the II2rb locus (encoding CD122, a chain of the IL-2 receptor); in turn, GC Tfh cells lacked expression of the IL-2 receptor and remained insensitive to IL-2.127. The gene discussed is IL2; the disease is influenza.