The etiological origin and the possibility of pharmacological intervention of autism represent two areas of great scientific interest and on which research has not yet provided conclusive results. However, as already highlighted by CREA in many publications on this site, there are more and more frequent studies that place in genetics some important causal and therapeutic principles. Joseph Glessner and his colleagues in the Children’s Hospital of Philadelphia, comparing the genomes of 859 autistic children with that of 1409 healthy children, have identified among the most frequent genes implicated in the development of autistic disorder, those that regulate the adhesion between nerve cells (NLGN1, ASTN2) and those responsible for the production of ubiquitin (UBE3A, PARK2, RFWD2, FBXO40), a protein involved in the reduction of superficial proteins that promote cell adhesion. Dan Ehninger and Alcino Silva of the University of California, Los Angeles, have conducted an experimental study that brings an important contribution to the potential of pharmacotherapy in the treatment of autism. These researchers have found that a sample of mice with tuberose sclerosis, a disease of genetic origin that in men is associated with autism in 50% of cases, the administration of rifampicin, a drug used to reduce the risk of transplant rejection, it seems to reduce cognitive deficits. Although it does not represent the discovery of a medication for autism, for the first time this study seems to support the theory that the alteration of cognitive functions of neurodevelopmental disorders are not irreversible.The ability to modulate through pharmacological principles the expression of genes is supported by other studies, even in areas different from that of autistic spectrum disorders, and is in line with the principles of epigenetics.The latter is a branch of genetics, that studies the ability of the environment, both internally and externally to living organisms, to induce transformation not definitive of DNA or RNA, to vary the gene expression and modify in this way the functioning of those same organisms.