Ovarian cancer is the foremost cause of death from gynecological cancer in the developed world. In the USA 27,000 new cases of ovarian cancer and 14,000 deaths are reported in 2010. About 80% of patients with ovarian cancer present with metastatic disease. The overall 5-year survival rate for women with cancer is 30%. The epithelial cells of the ovary constitute 1% of the total ovarian mass but constitute 90% of the ovarian neoplasms. Epithelial ovarian cancer (EOC) spreads initially by direct extensions into adjacent organs, especially the fallopian tubes, uterus and contralateral adnexa and occasionally the rectum, bladder and pelvic side wall. After direct extension, epithelial ovarian cancer frequently disseminates via transcoelmic route, with 70% of patients having peritoneal metastases at staging laparotomy. The correlation between molecular profiles and metastatic spread varies depending on tumor type and metastatic site and is combination of 2 models. First, tumors are genetically heterogeneous and that metastases arise from clones with a genetically acquired metastatic phenotype and that the clonal genotype determines the final site of metastases. The second model is that metastatic cells are not a genetically primary tumor, instead they arise as stochastic event, with a low but finite probability from tumor cell clones distinct from the primary tumor. Several cofactors, such as MMP-2/-9 inhibitor, TNF, lypmphotoxin a, Fas Ligand Fas L, APO3L, TRAIL, interleukin -8 and P38 MAPK regulating ovarian cancer cells attachment to omentum and /or peritoneum have been identified and would have noticeable clinical inhibition of the metastatic process, by enabling the identification of cellular or molecular targets that therapeutically viable. That would be able to block the steps necessary for ovarian cancer metastasis within the peritoneal cavity.