Altered FLNA in AD aberrantly links to the α7 nicotinic acetylcholine receptor (α7nAChR) to enable the toxic signaling of soluble amyloid through this receptor to activate kinases (Dineley et al., 2002; Nagele et al., 2002; Wang et al., 2003) that hyperphosphorylate tau, leading to neurodegeneration, tau-containing tangles, and even intracellular Aβ42 aggregates and amyloid plaques (Wang et al., 2012; Wang et al., 2017; Burns et al., 2023). The gene discussed is CHRNA7; the disease is Alzheimer disease.