BCO2 and Alzheimer disease: Potential off-target hits, relatively low target expression in proliferating SH-SY5Y cells/in CNS, incomplete knockdown, or being a regulator of amyloid-β rather than tau may explain why not all MPxgb(AD) predicted genes showed an effect in reducing/increasing inflammation-induced tau phosphorylation (e.g., BCO2, Supplementary Fig. 4).