The ability to detect double-stranded (ds)RNA as a signature of viral infection is an evolutionarily conserved feature of innate immunity. However, animal genomes also express long dsRNA molecules capable of activating immune sensors. To avoid harmful inflammation, cells carefully control dsRNA levels, localisation and its exposure to sensors. The RNA editing enzyme, ADAR1, directly modifies dsRNA by converting adenosine to inosine (A-to-I editing), which suppresses dsRNA sensor activation to prevent autoinflammation. Using loss of editing by ADAR1 as a model and genome-wide CRISPR screening, we identified new cellular regulators of dsRNA (Science Immunology, 2024). We identified a new function for the cyclin-dependent kinase, CDK13, in dsRNA sensing. CDK13 is a regulator of transcription elongation, and we hypothesise that loss of CDK13 reduces the dsRNA content of cells and/or results in aberrant proteins or RNAs that suppress dsRNA sensing, allowing a cell to tolerate loss of A-to-I RNA editing. Understanding new mechanisms of dsRNA control present new opportunities to manipulate the immune response to RNA, of relevance to autoinflammatory disease and cancer immunotherapy.