The dualistic model of EOC tumor development suggests that a large portion of high grade EOC tumors (G2 and G3) arise from the ovarian epithelium cells by as yet not clear mechanism implicating TP53, BRCA1 and/or BRCA2 mutations [63], whereas the LG TOVs (grade 1) arise from a sequence of unknown molecular events beginning with the development of BOV, transitioning through to LMP and MPSC before ending with a LG TOV tumor [63,64]. Here, TP53 is linked to neoplasm.