Melanocyte-specific loss of p16INK4a and activation of K-Ras promoted the development of melanomas [90]; B-cell specific inactivation of CDKN2A and activation of K-Ras promoted the development of highly aggressive B-cell acute lymphoblastic leukemia [91]; and alveolar-specific inactivation of CDKN2A and activation of K-Ras promotes development of lung adenocarcinomas [92]. The gene discussed is KRAS; the disease is lung adenocarcinoma.