A possible explanation for this finding is that similar to that observed in NSCs104, a sustained high level of ASCL1 leads to an upregulation of Hes5 (Fig. 6j), which in turn downregulates Olig227,28, as revealed at both the transcript and protein levels in Ascl1-OE compared to control and Ascl1-CKO tumor cells (Figs. 3g, 8a). The gene discussed is ASCL1; the disease is neoplasm.