CAMK2A and glioblastoma: To address these three crucial questions, the LN229 and U87MG glioblastoma cells were pre-treated separately with: (1) Dextromethorphan (DXM, 10 μM) to inhibit NR2B receptor phosphorylation which will prevent extracellular calcium influx (Marquard et al., 2015); (2) Calmodulin binding domain peptide (CAMBD, 200 nM) that sequesters calmodulin cellular pool and also acts as a pseudo-substrate and suppress CaMK2A phosphorylation (McCoy et al., 2013); and (3) BAPTA (20 μM) to chelate intracellular calcium which would inhibit CaMK2A phosphorylation (Figure 10A).