While it remains to be established whether astrocyte reactivity is an early causal driver of AD, the associations of elevated plasma GFAP levels with severity of both neuritic plaque and neurofibrillary pathology as well as with pTau and NfL levels suggest that it may be important both as a potential initiator of AD pathogenesis as well as a plausible mediator of intermediate and late stages of AD progression. The gene discussed is GFAP; the disease is Alzheimer disease.