Consistent with the inability of SLE patient BLK variants to repress IFNb, examination of peripheral blood mononuclear cells from family G patients heterozygous for the BLKR238Q variant (G.I.1, G.II.1, G.II.2, and G.II.3) revealed upregulation of the T1 IFN signature (Fig. 4c and module M1.2 in Fig. 4d) as well as apoptosis/survival pathways (module M6.6 in Fig. 4d, Supplementary Fig. 5). This evidence concerns the gene IFNA1 and systemic lupus erythematosus.