Interestingly, our findings demonstrate a strong affinity of RA towards both BACE1 and synapsin I. Therefore, we postulated RA as a promising agent that can suppress abnormal Aβ production by targeting BACE1 and synapsins in AD, however, further in vivo and in vitro studies on the molecular interactions are warranted. The gene discussed is BACE1; the disease is Alzheimer disease.