In order to confirm the involvement of β1-integrin in the therapeutic effects of NX210 and NX210c in AD, we would need to determine the following: (i) whether levels of β1-integrin are differentially modulated in neurons (decrease) and astrocytes (increase) in the Aβ25–35 mouse model used in this study and (ii) whether NX210 and NX210c prevent cofilin activation and decrease the levels of FAK (in neurons) and NOX2 (in astrocytes) in the prefrontal cortex and hippocampus of Aβ25–35-injected mice. The gene discussed is PTK2; the disease is Alzheimer disease.