The conclusion of these recent studies of "de novo" mutation is that the spectrum of autism is breaking up into quanta of individual disorders defined by genetics. One gene that has been linked to autism is SHANK2. Mutations in this gene act in a dominant fashion. Mutations in this gene appear to cause hyperconnectivity between the neurons. Epigenetic mechanisms may increase the risk of autism. Epigenetic changes occur as a result not of DNA sequence changes but of chromosomal histone modification or modification of the DNA bases. Such modifications are known to be affected by environmental factors, including nutrition, drugs, and mental stress. Interest has been expressed in imprinted regions on chromosomes 15q and 7q. Most data supports a polygenic, epistatic model, meaning that the disorder is caused by two or more genes and that those genes are interacting in a complex manner. Several genes, between two and fifteen in number, have been identified and could potentially contribute to disease susceptibility. However, an exact determination of the cause of ASD has yet to be discovered and there probably is not one single genetic cause of any particular set of disorders, leading many researchers to believe that epigenetic mechanisms, such as genomic imprinting or epimutations, may play a major role. Epigenetic mechanisms can contribute to disease phenotypes. Epigenetic modifications include DNA cytosine methylation and post-translational modifications to histones. These mechanisms contribute to regulating gene expression without changing the sequence of the DNA and may be influenced by exposure to environmental factors and may be heritable from parents. Rett syndrome and Fragile X syndrome (FXS) are single gene disorders related to ASD with overlapping symptoms that include deficient neurological development, impaired language and communication, difficulties in social interactions, and stereotyped hand gestures. It is not uncommon for a patient to be diagnosed with both ASD and Rett syndrome and/or FXS. Epigenetic regulatory mechanisms play the central role in pathogenesis of these two diseases. Rett syndrome is caused by a mutation in the gene that encodes methyl-CpG-binding protein (MECP2), one of the key epigenetic regulators of gene expression. MeCP2 binds methylated cytosine residues in DNA and interacts with complexes that remodel chromatin into repressive structures. On the other hand, FXS is caused by mutations that are both genetic and epigenetic. Expansion of the CGG repeat in the 5’-untranslated region of the FMR1 genes leads to susceptibility of epigenetic silencing, leading to loss of gene expression.