These alterations were shown to facilitate the adhesion of ovarian cancer cells mainly via (i) exposure of submesothelial ECM, where cancer cells preferably adhere, and via (ii) upregulated expression of ICAM-1/VCAM-1, HA, and FN1, providing integrin- and CD44-mediated ovarian cancer cell adhesion [11,17,18,22,26–29]. This evidence concerns the gene ICAM1 and ovarian carcinoma.