Since cellular levels of methylglyoxal in the brain during neurological disease are not established, it is possible that the 100 μm methylglyoxal required to increase cellular MG-H1 and produce AIS shortening in the current in vitro study does not represent pathophysiological levels in vivo. Nevertheless, it is reasonable to think that prolonged increase of methylglyoxal, or the combined disruption of methylglyoxal, insulin, and glucose metabolism, during type 2 diabetes could result in sustained AIS shortening and CNS dysfunction. The gene discussed is INS; the disease is type 2 diabetes mellitus.