Midkine (MDK) is a heparin-binding growth factor that is highly expressed in many malignant tumors. MDK activates the PI3K pathway and induces anti-apoptotic activity, in turn enhancing the survival of tumors. Therefore, the inhibition of MDK is considered a potential strategy for cancer therapy. Midkine (MDK) and the related heparin-binding growth associated molecule (HB-GAM)/Pleiotrophin (Ptn) are widely expressed in healthy cells as well, and are involved in a wide range of biological processes. Originally identified as retinoic acid inducible genes, midkines are widely expressed during embryogenesis with particularly high levels in the developing nervous system. During postnatal stages, midkine expression generally ceases but is often up-regulated under disease conditions, most notably those affecting the nervous system. Midkines are known as neurotrophic factors, as they promote neurite outgrowth and neuron survival in cell culture.  In addition, several studies reported that MDK and Ptn acted as survival factors for neurons and that this activity was mediated through inhibition of apoptosis by modulating the MAPK pathway. Evidence was found that inhibition of MDK or its putative receptor anaplastic lymphoma kinase (Alk) results in reduced proliferation and induced apoptosis, hence further supporting the role of MDK as survival factor for neurons and a crucial factor for neurogenesis in vivo.[1]