In order to confirm that akin to BM treatment, Bacoside A itself can extensively phosphorylate the CaMK2A pool in various glioblastoma cells with different genetic landscapes, we treated the normal human cells: SVG-subventricular zone derived glial cells; HaCaT-epidermal keratinocytes and various GBM patient derived tumor cell lines: U87MG, U251 and LN229 with Bacoside A (8 μg/ml) treatment for 24 h (Figure 9A). This evidence concerns the gene CAMK2A and neoplasm.