Taken together, these mouse or in vitro carcinogenesis models support the concept that a total of 3 genetic hits are required for the development of HGSC from FTSECs, in which TP53 mutation is indispensable and the additional 2 hits, including BRCA mutation (or HRD), PI3K‐APT, Ras‐MAPK signaling, or c‐Myc amplification (overexpression), confer the serous carcinoma phenotype. Here, TP53 is linked to serous adenocarcinoma.