KRAS and adenocarcinoma: The potential importance of secondary somatic mutations in promoting oncogenic K-ras-induced lung tumorigenesis is illustrated by the long latencies of adenocarcinomas that arise in mice engineered to express mutant K-ras, which develop lung lesions rapidly and with high penetrance, but only a fraction of the lesions progress into adenocarcinomas and require several months to do so [3]–[7].