A multi‑institutional study published in Cell revealed that high MYC expression enables tumors to evade innate immune sensing by binding nascent RNA, recruiting the nuclear exosome and degrading R‑loop–derived RNA–DNA hybrids that would otherwise activate antiviral signaling. Researchers from the University of Würzburg, MIT and Würzburg University Hospital showed that MYC’s RNA‑binding multimers prevent accumulation of immunostimulatory hybrids and blunt TBK1/TLR3‑mediated innate responses. The work identifies an RNA‑binding, exosome‑recruiting function of MYC distinct from its canonical transcriptional role and suggests new vulnerabilities in MYC‑driven cancers. Translationally, the findings nominate approaches aimed at disrupting MYC’s RNA interactions, modulating R‑loop processing, or harnessing innate sensing as potential combination strategies to re‑sensitize tumors to immunosurveillance.