Interestingly, another mouse model under study, which bears an activating Q72L mutation in Rras2, develops different types of cancer but not breast cancer [56], suggesting that the capacity of the wild-type R-RAS2 protein to cycle between the GTP-bound and the GDP-bound states might allow the emergence of tumors that otherwise would be locked if R-RAS2 is in the permanently active conformation. The gene discussed is RRAS2; the disease is breast carcinoma.