COL6A2 and Dravet syndrome: For example, COL6A1 and COL6A2 were highly expressed in DS fetuses, and their overexpression was closely linked with congenital defects in DS [46–48]; MX1 and MX2 were highly expressed in DS blood cells and involved in the interferon signaling pathway [12], which is regarded as one of the determined factors in infections and immunodeficiency, aging, and microglial dysfunction in DS [49–52].