In the present work, we have sought to investigate the role of RhoA and the closely related Rho GTPase, RhoC, in K-Ras-induced tumorigenesis using a well-established inducible K-RasG12D knock-in mouse model of lung adenoma induction in combination with our RhoA conditional knockout, RhoAflox/flox, and RhoC-/- mouse models. This evidence concerns the gene KRAS and lung adenoma.