Even if SAP is required in CD4 T cells for GC responses, SAP-deficient mice develop normal numbers of CXCR5high ICOShigh putative TFh cells. Thus, the precise role for SAP has been elusive. In an interesting study Shane Crotty and colleagues have shed light on the complexity for the requirements for SAP. As markers have been lacking to distinguish between TFh and GC CD4 T cells, data from this study improve our knowledge of GC-TFh cells. They have identified CXCR5high GL7high CD4 T cells as a sub-population of TFh cells localised within GC. GL7, which has long been used to mark GC B cells, now allows the distinction between GL7high GC-TFh cells and GL7low non-GC-TFh cells. Importantly they show that SAP-deficient T cells are impaired in their development into GL7high GC-TFh cells, reconciling the discrepancy between the normal development of TFh cells but defect in GC response obtained in SAP-deficient mice. In addition, a challenging result from this study is that in response to LCMV infection, a potent Th1-inducer, IL-4 mRNA expression was detected in the GL7high GC-TFh cell population. They show that CD150 SLAM is the primary receptor responsible for driving IL-4 production by GC TFh cells during this viral infection. Finally, CD150 is also required to induce IL-21 mRNA by this the GL7high GC-TFh cell population.