Recent work by our laboratory elucidated a potential pathophysiologic relationship between elevated fibronectin levels and Aβ1–40 deposition in vivo, finding that intracisternally infused CSF Aβ1–40 deposited within thickened, fibronectin-rich segments of the BM in aged mice with stroke, and that fibronectin-Aβ1–40 conjugation increased its deposition within the BM of pial vessels (Howe et al., 2018a). The gene discussed is FN1; the disease is Stroke.