According to this system, Type 2 cancers, encompassing the clinically more aggressive high-grade serous carcinomas, are defined by frequent mutations in p53 and BRCA1/2 genes, leading to genomic instability, while type 1 tumours, encompassing low-grade serous and endometroid carcinomas, clear cell, mucinous and transitional cell (Brenner) tumours, are characterized by common KRAS mutations [8,9]. The gene discussed is KRAS; the disease is serous adenocarcinoma.