Previous research discovered that SAP protein was downregulated in CTLs while the SLAM protein 2B4 was upregulated in patients with congenital PI3K deficiency disorder such as activated PI3Kδ syndrome, implying that SAP may interact with PI3K-associated pathways and XLP-1 may be related to PI3K signaling failure.[19] Insight details of the interaction patterns between SAP and PI3K, as well as the role of PI3K-associated pathways in pathogenesis of XLP-1 still need to be investigated further. Here, SH2D1A is linked to X-linked lymphoproliferative disease.