By comparing the activity of wild type (WT) and of a phospho-mutant form of ASCL1 that cannot be phosphorylated on SP consensus sites, we show that inhibition of ASCL1 phosphorylation increases the fraction of cells expressing neuronal markers and drives GBM cells to a post-mitotic neuronal-like state that is refractory to cell cycle re-entry upon growth factor stimulation. The gene discussed is ASCL1; the disease is glioblastoma.