A Cell paper from teams at the University of Würzburg and MIT reported that high levels of MYC bind nascent RNA, recruit the nuclear exosome, and clear R‑loop RNA–DNA hybrids—silencing innate immune signaling and enabling tumor immune evasion. The mechanistic insight identifies MYC’s RNA‑binding regions as separable functions from its transcriptional roles. In related work, investigators from Memorial Sloan Kettering and collaborators characterized a high‑plasticity tumor cell state that drives drug resistance and progression, and highlighted targetable pathways linked to metabolic and epigenetic remodeling. What happened: Two studies revealed noncanonical mechanisms—MYC‑mediated R‑loop clearance and plasticity‑driven adaptation—that tumors use to escape therapy and immune detection, offering fresh molecular targets. Sources: Cell, Molecular Cancer reporting, and institutional releases. Research note: these findings point to strategies that combine immune‑stimulatory approaches with inhibitors of RNA‑processing or plasticity pathways.