The specific goals of this review are to discuss the shared characteristics and pathology of AD and T2DM, explain some of the possible pathological mechanisms that can contribute to cognitive dysfunction in both diseases (i.e., insulin resistance and impaired signaling, inflammation), and in light of these points, discuss potential novel treatment targets and interventions that could prove useful in improving cognition and quality of life for those suffering from AD. The gene discussed is INS; the disease is Alzheimer disease.