If cells fail to pass through the developmental window of transient high ASCL1 expression, followed by differentiation and subsequent ASCL1 downregulation, these elevated levels of phosphorylated ASCL1 would cause NB precursors to remain in cycle, and cells would be able to accumulate further epigenetic or genetic ‘hits’ such as MYCN amplification and chromosomal rearrangements, driving tumour progression. This evidence concerns the gene MYCN and neoplasm.