Neuroblastoma, the third most frequent childhood tumor, accounts for 15% of childhood cancer mortality. In-depth knowledge of ALK downstream signaling and identification of new vulnerable nodes for treatment is needed in order to design multi-compound oriented treatment. It is anticipated that such therapy can drastically reduce the chances of acquiring resistant phenotypes. In order to optimize targeted treatment, this project will further study growth promoting signaling in neuroblastoma cells carrying the ALKF1174L mutation as well as the molecular basis underlying the cooperative oncogenic effect between ALKF1174L mutation and MYCN amplification.