KRAS and lung adenoma: Mice of the K-RasLA strain, in which expression of K-RasG12D can be spontaneously activated by random recombination, develop lung adenomas.12 Similarly, in a LoxP-Stop-LoxP-K-Ras conditional mouse strain (K-RasLSL-G12D), expression of oncogenic K-Ras is controlled by a removable transcriptional termination Stop element; when the expression of endogenous level of K-RasG12D was triggered in lung by Adeno-Cre-mediated deletion of the Stop sequence, the mice developed adenomas in a month of stimulation.10, 41