STAT1 GOF mutations are all AD and result in an increased responsiveness to both type I and type II IFNs, as well as IL-27 [46], as a consequence of more rapid and sustained STAT1 tyrosine phosphorylation and nuclear accumulation mediated by several mechanisms, including increased levels of STAT1 and other signaling proteins [46,49,50,51]. Here, STAT1 is linked to Alzheimer disease.