Although much remains to be investigated in various directions, it is tempting to generalize these findings on a number of levels. Etiologically, rare and private mutations clustered in select molecular classes appear to be a major driver for a genetic basis in a sub-set of ASD patients. At the molecular level, several pathways appear to emerge from analyzing the existing ASD mouse models. These include disruption of overlapping signaling pathways mediated by mGluR5, BDNF, and mTOR (see Figure 1 and Table 2), although the degree of evidence varies depending on the model.
