In a transgenic zebrafish model of NB in which MYCN-induced tumors arise from a subpopulation of neuroblasts, co-expression of activated ALK with MYCN triples the disease penetrance and markedly accelerates tumor onset by providing pro-survival signals that block the physiological apoptotic response and allowing for continued expansion and oncogenic transformation [184]. The gene discussed is MYCN; the disease is neuroblastoma.