Based on these findings, we hypothesize that FcγR-mediated phagocytosis could be a central pathway in the LQZ treatment for AD, with Fcgr3, Tyrosine-protein kinase (Syk), Phosphoinositide phospholipase C-gamma-2 (Plcg2), V-yes-1 Yamaguchi sarcoma viral related oncogene homolog (Lyn), Neutrophil cytosol factor 1 (Ncf1), Ras-related C3 botulinum toxin substrate 2 (Rac2) and Actin-related protein 2/3 complex subunit 3 (Arpc3) emerging as key proteins (Table 2, up-regulated in DNCB group and down-regulated in LQZ-H group). Here, ARPC2 is linked to Alzheimer disease.