Memorial Sloan Kettering researchers reported in Nature Cancer that disseminated lung adenocarcinoma cells use a TGFβ-driven program to enter dormancy and adopt a rounded morphology that reduces surface tension, helping them evade cytotoxic T lymphocytes. The team, led by Joan Massagué and Zhenghan Wang, showed the atypical EMT transition produces a soft, round state resistant to immune mechanosurveillance in mouse models. The study links phenotypic plasticity to immune escape during dormant metastasis and suggests strategies to prevent or reverse the soft state—re-stiffening cells or blocking the transition could expose dormant cells to clearance. Findings highlight a mechanobiology axis in metastasis that may inform adjuvant approaches to prevent late relapse.