Recent data support a central role for astrocyte dysfunction early in AD pathogenesis, for example, via an association of astrocyte-enriched SNPs with early amyloid pathology [6], as well as changes observed to both MOA-B PET tracer positivity [7] and plasma levels of GFAP [8] prior to amyloid plaque formation. The gene discussed is GFAP; the disease is amyloidosis.