The total penetrance of this phenotype (25/25 mice), together with the rapid development of the oral tumours, suggests that few additional mutations or epigenetic changes are required for mutant K-ras-induced oral squamous hyperplasia and papilloma formation with neoplasia, supported by CGH analysis of tumours from these mice revealing no gross genomic instability (Supporting information, Supplementary Figure 1). The gene discussed is KRAS; the disease is neoplasm.