Based on this finding, Hoirisch-Clapauch et al. hypothesized that neuronal dis-connectivity due to abnormal neuronal migration underlies the development of ASD, and that fetal hyperglycemia increases PAI-1 levels causing the inhibition of tPA activity for reelin glycoprotein, which guides neurons and glial cells from the ventricular zone to the cortex [42]. The gene discussed is SERPINE1; the disease is Hyperglycemia.