Genomes were scanned using the Infernal program. The identified candidate RNA regulatory sites for each riboswitch family were uploaded into the RegPredict Web server and the respective RNA regulogs were reconstructed using the same approach as for TF regulogs. New regulatory RNAs were found by groups of genomes. Secondary structures of two alternative RNA conformations were predicted using Zuker’s algorithm of free energy minimization implemented in the Mfold Web server. To assess conservation of regulatory interactions in the reconstructed orthologous regulogs we calculated the conservation score as the number of gene occurrences in a regulog divided by the number of regulons in a regulog. The average of these taxonomy-specific conservation scores was calculated for all taxonomic groups where the regulated gene was observed. For each TF, we ASP1517 plotted the average conservation scores for all regulatory targets against the number of taxonomic groups, in which this target was observed as regulated. These plots were used to determine the core, well-conserved, taxon-specific and genome-specific target genes within the analyzed regulons. The details of all reconstructed TF- and riboswitch-controlled regulogs are deposited in the RegPrecise database. Sequence logos for the derived TFBS motifs were built using the Weblogo 3 package. Biological functions of genes in the reconstructed regulogs were predicted by sequence similarity search against the Swiss-Prot/UniProt database, domain architecture analysis in the Pfam database, and by using functional gene annotations from the SEED and KEGG. Autism is a clinically complex, heterogeneous, and behaviorally-defined neurodevelopmental disorder characterized by impaired social skills, communication, and repetitive behaviors. Substantial effort has been devoted in recent years to uncover the underlying mechanisms of genomic, epigenomic, proteomic, metabolic, and physiological alterations associated with the disease development. Although the role of genetic factors in autism has been extensively studied, the genetic variations are extremely heterogeneous and their phenotypic penetrance is highly variable in different individuals. In addition to genetic alterations, mounting evidence indicates a key role of other molecular and physiological abnormalities, including immune dysregulation, neuroinflammation, epigenetics, oxidative stress, and mitochondrial dysfunction ; however, the underlying molecular pathogenesis of autism remains elusive. In recent years, the cerebellum has emerged as one of the key brain regions affected in autism. This is evidenced by several well-established observations indicating the essential role of autism in the development of basic social capabilities, its involvement in extensive neural networks that govern the social, communication, repetitive/restrictive behaviors, and motor and cognitive deficits impaired in autism. Elucidating and understanding the molecular processes underlying the pathogenesis of autism is critical for effective clinical management and prevention of this disorder. Investigation of these mechanisms using human subjects is desirable.