Although there is evidence that both common and rare disease susceptibility loci are likely to converge on specific molecular and biological pathways in ASD and potentially SCZ (64), many issues remain. The pathways as currently defined are broad and should be refined at the level of protein function and cellular signaling to obtain more specific insight into disease pathogenesis. Furthermore, knowing how these pathways reflect genetic risk at the level of individuals is necessary to develop a mechanistic understanding of disease.
