Supporting this hypothesis is a recent report demonstrating that overexpression of three neurogenic transcription factors (achaete-scute complex homolog 1 (ASCL1), BRN2 and NGN2) in cultured human glioma cells is able to convert 20–40% of them into βIII-tubulin (TUBB3, also known as TUJ1)-positive neuron-like cells.23 To effectively inhibit tumor growth, however, much higher conversion efficiency will be essential. This evidence concerns the gene ASCL1 and neoplasm.