More recently, the same group used the same system to express Activated Mek (MAPK/extracellular signal‐regulated kinase (ERK) kinase (MEK), a RAF effector), to induce tumours in vivo in the context of activated Akt or INK4a/Arf loss, showing that indeed activated MEK cooperates with Ink4a/Arf loss or Akt activation to induce gliomas in vivo [98]. Here, CDKN2A is linked to glioma.