Emerging evidence suggests that intron-detaining transcripts are a nucleus-detained, polyadenylated, and post-transcriptional mRNA pool essential for cell to quickly respond to environmental stimuli and stress. Meng et al. demonstrated that the detained intron (DI) splicing is paused at Bact state, an active spliceosome but not catalytically primed, which differs from constitutively splicing introns that are co-transcriptionally spliced. RNPS1 recognizes the DIs and its neighboring sequences through its RRM (RNA recognition motif), which is sufficient to induce the intron detention. SNIP1 forkhead-associated domain and RNPS1 serine-rich domain are required not only for their interaction but the intron detention. SNIP1 knockout decreases DI splicing and causes neurodegeneration, likely through sequester of spliceosome pausing complex, a new molecular mechanism for neurodegenerative diseases.