Researchers at Memorial Sloan Kettering Cancer Center reported that TGFβ signaling induces an atypical epithelial‑to‑mesenchymal transition that ultimately converts disseminated lung adenocarcinoma cells into a rounded, low‑tension state that resists cytotoxic T‑cell killing. The study, published in Nature Cancer, traces how TGFβ‑dependent programs lead to growth arrest, EMT and a subsequent soft morphology that impairs immune mechanosurveillance. Authors Joan Massagué and Zhenghan Wang led experiments in mouse models demonstrating that the softened state reduces immune cell‑mediated membrane disruption. The team proposes mechanically targeted interventions—either preventing the soft state or restoring cell stiffness—to expose dormant cells to immune clearance. One‑sentence clarification: epithelial‑to‑mesenchymal transition (EMT) describes cellular programs that change adhesion and shape, affecting migration and immune visibility. The findings outline a biophysical immune‑evasion mechanism with direct implications for adjuvant strategies aimed at eradicating dormant metastatic reservoirs.