AKT1 and astrocytic tumor: The RCAS/tv‐a model yields astrocytic tumors (∼25% incidence in 12 weeks) in the N‐tva background when constitutively active variants of both kRas and Akt are used in combination as oncogenic drivers (34), and deletion of Pten in these mice appears to phenocopy the effects of RCAS‐mediated Akt overexpression (36).