Indeed, there is no current evidence to support that even long-term acetylcholinesterase inhibitor treatment affects such metabolites in AD patients, and additionally, several of the top metabolite markers identified were either directly already known to be associated with AD (L-tyrosine) or involved in oxidative damage of proteins (3-chlorotyrosine) which is itself a marker of AD [37]. The gene discussed is ACHE; the disease is Alzheimer disease.