STAT1 and Aicardi-Goutieres syndrome: Similar to chronic IFN-I stimulation in vitro [12], tyrosine phosphorylation of residue Y690 on STAT2 (but not pY701-STAT1) was decreased in unstimulated CD14+ monocytes of AGS patients with mutations in SAMHD1, RNASEH2B, and TREX1 (Fig. 4b).