In three other ovarian cancer cell lines (OC 314, OC 315, OC 316), it was demonstrated that CXCL12/CXCR4 interaction induces a dose-dependent cell proliferation through ERK1/2 and Akt activation that was dependent on EGFR phosphorylation caused by a mechanism involving the activity of the cytosolic tyrosine kinase c-Src [40]. This evidence concerns the gene AKT1 and ovarian carcinoma.