For Investors - Application software
We have written a rather large Windows desktop application called SAITO  (斎藤; Japanese for wisteria) that currently has almost 500 forms and almost 200,000 lines of code. It is intended to support teachers, parents, social service workers, graders, physicians and other interested parties such as students, martial arts instructors, grandmasters and investors.
Currently, SAITO does support diagnoses below the level of individual genes. That means specific mutations or micro-deletes or nucleotide repeats can be associated with a student. Generally, the field of human genetics can be judged
to be in transition when it comes to asociating genes and mutations with syndromes and disability categories. At present there are at least 54 known mutations of the FOXP2 gene. FOXP2 is normally located in the q31.1 region – a translocation to the q22 region causes a condition known as developmental verbal dyspraxia (DVD). Both a missense mutation causing an arginine-to-histidine substitution (R553H) and a nonsense mutation (R328X) causing a truncated protein cause speech and language difficulties. FOXP2 also regulates at least the following genes: SRPX2 (work underway); CNTNAP2 and CTBP1. CNTNAP2 interacts with CNTN2. CNTN2 interacts with the NFYB gene which interacts with three more genes. Of those, CEBPZ interacts with 2 other genes, myc with 37 other genes and TBP with 27 other genes. CTBP1 interacts with 14 other genes. The second generation of interactions with the CTBP1 gene now includes over 160 other genes.

So far, 240 genes linked to FOXP2. It appears that simply searching for other students with the R553H mutation of the FOXP2 will not suffice. SAITO will have to find a way to link, for example,  FOXP2 and CTPB1 as well as FOXP2 and other genes that cause similar symptoms. We expect major regrouping of syndromes and perhaps even some categories. At some point a system like the one used to name R553H will likely arise to describe epigenetic influences like DNA methylization and histadone modifications.
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