A more recent study utilized an activating PIK3CA mutation (the mutation alone induced premalignant hyperplasia of the OSE, but not tumors) coupled with PTEN loss in the mouse ovary to drive the formation of ovarian carcinoma from the OSE: the double-mice mutant developed ovarian serous adenocarcinomas, granulosa cell tumors and luteoma tumors [308]. This evidence concerns the gene PTEN and ovarian carcinoma.