It has been demonstrated that the exposure of microglia to soluble factors released by glioma cells induces the activation of the PI3K/Akt and FAK pathways and that these signaling pathways are involved in cell movement and phagocytosis.22, 23 Having demonstrated that anti-inflammatory microglia have increased migratory and phagocytic activity (Figure 4c) and higher functional expression of kcnn4 (Figure 3), we wanted to verify the hypothesis that KCa3.1 activity could contribute to the phenotype switch of microglia through the modulation of these signaling pathways. The gene discussed is AKT1; the disease is glioma.