The above findings suggest that continued or compensatory upregulation of key signaling molecules during crizotinib treatment could contribute to the limited activity of this agent against NB cells expressing ALKF1174L with concomitant overexpression of MYCN. To address this issue, we screened several mTOR, PI3K and dual PI3K/mTOR pathway inhibitors in NB cells (Table S2), identifying Torin1 [16] and Torin2 [17] as promising candidates. Here, MTOR is linked to neuroblastoma.