These include: (i) Amplification of MYCN on 2p24, a master regulator that sustains the NB cells growth, and repress their differentiation, thus being associated with an unfavorable prognosis [3]; (ii) gain of function of ALK, also located at 2p, whose expression is limited to neural tissues and is considered a predisposition gene being involved in the majority of familial NB and 10–15% of sporadic ones [4]. Here, ALK is linked to neuroblastoma.