To elucidate the signaling pathways by which overexpression of FAK leads to enhancement of the AD-like phenotype in 3xTg-AD mice, we performed enrichment analysis of the proteins in all four groups (control non-stimulated, control stimulated, FAK-OE non-stimulated, and FAK-OE stimulated) which were pairwise compared. The gene discussed is PTK2; the disease is Alzheimer disease.