In other words, the differential sensitivity to GSI does not stem from any particular molecular characteristic of GSCs or U87 cells (in both, invasive potential of ADAM23hi cells are not sensitive to GSI), but rather it derives from ADAM23 knockdown, supporting the thesis that GS is activated by the downregulation of ADAM23 in astrocytoma cells. Here, ADAM23 is linked to astrocytoma (excluding glioblastoma).