Previous studies suggest the presence of a minicolumnopathy in autism. Minicolumnar abnormalities as well as certain migratory and proliferative defects, common to autism, may be rooted in the general mechanics of periventricular germinal cell division and maturation. Increased numbers of periventricular germinal cell/radial glia can be mimicked by a variety of different transgenic mouse models and environmental factors. These murine models and environmental factors illustrate how a fairly homogenous neuroanatomical phenotype can diverge at the genetic level. By first defining the lowest common denominator (i.e., the minicolumn) and then examining which pathways are vulnerable to involved genetic and environmental factors, we may gain a greater understanding of the pathophysiologic mechanisms underlying Autism Spectrum Conditions.