A genome‑wide screen at A*STAR IMCB uncovered a P2Y2‑integrin β1 axis that stabilizes mutant EGFR proteins in non‑small cell lung cancer. The team showed that tumor cells secrete ATP to activate P2Y2, recruiting integrin β1 and blocking mutant EGFR degradation; genetic disruption of this axis led to loss of mutant EGFR and tumor shrinkage in models. Authors highlighted P2Y2 as a cell‑surface target that could be drugged to overcome resistance to EGFR inhibitors; findings were published in Science Advances.