Overall, the most common gene mutations in ovarian cancer occur in "NF1, BRCA1, BRCA2, "and "CDK12". Type I ovarian cancers, which tend to be less aggressive, tend to have microsatellite instability in several genes, including both oncogenes (most notably "BRAF" and "KRAS") and tumor suppressors (most notably "PTEN"). The most common mutations in Type I cancers are "KRAS, BRAF, ERBB2, PTEN, PIK3CA," and "ARID1A." Type II cancers, the more aggressive type, have different genes mutated, including "p53, BRCA1", and "BRCA2". Low-grade cancers tend to have mutations in KRAS, whereas cancers of any grade that develop from low malignant potential tumors tend to have mutations in p53. Type I cancers tend to develop from precursor lesions, whereas Type II cancers can develop from a serous tubal intraepithelial carcinoma. Serous cancers that have BRCA mutations also inevitably have p53 mutations, indicating that the removal of both functional genes is important for cancer to develop.