Thus, although we cannot rule out a requirement for other SLAM family members for GC responses, the defects observed in SAP-deficient mice and humans with XLP may well result from inhibitory signaling in the absence of SAP, as suggested by the rescue of GC formation in Slamf6-/-Sh2d1a-/- mice. Here, SH2D1A is linked to X-linked lymphoproliferative disease.