Together with the Aβ-lowering strategy, our results provide new ways for AD therapeutics to rescue Aβ and tau pathology: i) selective inhibition of the interaction between FcγRIIb and Aβ1-42, ii) inhibition of a kinase (i.e., Lyn) which phosphorylates FcγRIIb upon Aβ1-42 stimulation, and iii) inhibition of SHIP2 which disrupts phosphoinositide metabolism. This evidence concerns the gene INPPL1 and Alzheimer disease.