we found that the strongest signals came from ACTB, ARID2, BCL11A, BCL11B, BCL7B, BCL7C, DPF2, and DPF3. This combination of data provides growing support for the involvement of SWI/SNF chromatin remodeling in the development of AD. Importantly, our analyses indicate that association should be evaluated at the level of the complex, which is made up of the protein products of multiple genes, and that variation in different genes may be altering SWI/SNF activity across different samples.
