Two mechanistic cancer studies outlined how tumors evade therapy and immune detection. A Cell paper showed high‑MYC tumors suppress innate immune signaling by binding nascent RNA and recruiting RNA‑degrading complexes to clear R‑loop‑derived alarm signals, blunting TBK1/TLR3‑mediated antiviral responses. The study tied MYC’s RNA‑binding activity to immune evasion and identified potential vulnerabilities in MYC‑driven cancers. Separately, investigators at Memorial Sloan Kettering described a ‘high‑plasticity cell state’ that drives progression and drug resistance, mapping transcriptional programs that may be targetable to prevent lineage switching and therapeutic escape. Both teams report actionable mechanistic nodes—RNA‑processing/exosome recruitment and plasticity regulators—that could be pursued with drug discovery campaigns. Why it matters: these findings expose conserved, non‑genetic mechanisms tumors use to avoid immune surveillance and therapy. They provide concrete biochemical targets for companies seeking first‑in‑class agents to sensitize resistant tumors to immunotherapy and targeted drugs.