Although the cellular mechanisms through which IGFBP-2 exerts a role in ovarian tumorigenesis are not completely elucidated, experimental data demonstrate that the growth-modulating effects of IGFBP-2 in ovarian cancer cells may be mediated by the activation of three specific cascades controlling cell growth, proliferation, and differentiation, that is, extracellular signal-regulated protein kinases (ERKs), stress-activated protein kinases (SAPKs) or c-Jun N-terminal protein kinases (JNKs) and p38 kinases. This evidence concerns the gene IGFBP2 and ovarian carcinoma.