ALK and neoplasm: In vivo experiments confirmed that OTX015 prompted tumor regression in an EML4-ALK(+) NSCLC model, modulating both MYC and MYCN together with the down-regulation of several stem cells markers, in particular NANOG as well as Musashi-1, CD113 and EpCAM in NSCLC tumors, whereas little effect on other pluripotency genes such as Oct4, CD44 and CD24 was observed.