Metapristone, at low concentrations (<IC50) significantly reduced CXCL12-induced CXCR4 expression in ovarian cancer cells, and down-regulated the CXCR4-related mRNAs and intracellular proteins by interfering the CXCL12-activated Akt and ERK signalling pathways.108 Metapristone also inhibited the events of cellular invasion, migration, and adhesion. This evidence concerns the gene CXCR4 and ovarian cancer.