The normal cells were rather spared from this effect at a similar dose, probably due to adaptation of normal cells to higher pools of phospho-CaMK2A and the regulation of its phosphorylation by protein phosphatases in physiological situation vs. in glioma cells, and also probably due to the higher density of resident caveolae in normal cells (Sinha et al., 2011; Parton and del Pozo, 2013; Yeh et al., 2014; Echarri and Del Pozo, 2015; Zimnicka et al., 2016). The gene discussed is CAMK2A; the disease is glioma.