Braun et al provide evidence that in both human glioblastoma cells and murine neuronal progenitor cells, PRMT5 inhibition primarily disrupts splicing at detained introns, a distinct class of retained introns, yet exerts little influence on canonical alternative splicing events, including skipping of cassette exons (Braun et al, 2017). The gene discussed is PRMT5; the disease is glioblastoma.