The Ras subfamily of small GTP-binding proteins is frequently mutated in human cancers. Several lines of evidence suggest that Rac1 is required downstream of Ras-induced transformation. Kissil and colleagues combined conditional activation of K-ras with conditional deletion of Rac1 in a murine model of lung cancer and demonstrated that Rac1 is required for tumorigenesis in vivo. Shown are representative histological findings from K-ras^G12D; Rac1 ^{f lox/+} mice (bottom) or K-ras^G12D;Rac1^flox/flox mice (top) 12 weeks after induction of the tumorigenic program by infection with Adenovirus-Cre. These findings raise the interesting possibility that targeting Rac1 in Ras-mutated tumors may be therapeutically beneficial. For details, see the article by Kissil and colleagues on page 8089 of this issue.