Another protein that contributes to a lissencephaly disorder is DCX, or Doublecortin. DCX is a microtubule associated protein that is responsible for double cortex malformations. DCX is found in the second layer of the cortex, and in fact is still present in immature neurons of an adult cortex. It is thought that DCX affects neuronal migration through affecting the microtubule dynamics. Since DCX malformations results as a similar phenotype as with LIS1 malformations, it is thought they interact with one another on a cellular level. However, it is not yet known how this occurs. TSC, or tuberous sclerosis, is an autosomal dominate disorder. TSC1 or TSC2 inactivation can cause TSC and the associated tumors in the brain. When inactivation of TSC1 is present during corticogenesis, malformations of cortical tubers, or abnormal benign tissue growth, along with white matter nodes would form in mice. This replicates the effect TSC is found to have in humans afflicted with TSC. In the mice there would be a lack of GFAP in astrocytes however astrogliosis would not occur like in the human TSC. The sodium channel SCN3A has been implicated in cortical malformations . Recapitulation of corticogenesis in both human and mouse embryos have been accomplished with a three dimensional culture using embryonic stem cells (ESC). Recapitulation is the theory in which an organism passes through embryonic development in stages similar to evolution of that organism. By carefully using embryo body intermediates and cultured in a serum free environment cortical progenitors form in a space and time related pattern similar to "in vivo" corticogenesis. Using immunocytochemical analysis on mouse neural stem cells derived from ESCs, after 6 days there was evidence of neuronal differentiation. The recapitulation ability only follows after the knowledge of spatial and temporal patterns have been identified, along with giving the knowledge that corticogenesis can occur without input from the brain.