More specifically, in addition to activating mutations in either KRAS or BRAF, particularly in low-grade serous, endometrioid tumors, and mucinous tumors, alterations of genes encoding β-catenin (e.g., CTNNB1), CDKN2A, PIK3CA, and PTEN have also been found in a number of studies of type I lesions; mutations in TP53 are rarely seen in these tumors, with the exception of mucinous carcinoma in which TP53 mutations occur relatively frequently (Table 1) [15,18,21,24,25,29,33,34,35,36]. Here, TP53 is linked to mucinous neoplasm.