Akt is further activated by phosphorylation on a second residue (S473) via mTORC2 (in response to growth factors), p38/MK2 (MAPKAPK-2; in neutrophils and neuronal cells) or DNA-PK (in response to insulin, pervanadate in glioblastoma cells) [25]–[28]. Here, MAPKAPK2 is linked to glioblastoma.