A*STAR researchers identified a membrane‑proximal survival mechanism that stabilizes mutant EGFR in non‑small cell lung cancer: extracellular ATP activates the P2Y2 receptor, which recruits integrin β1 to shield oncogenic EGFR from degradation. The genome‑wide screen and tumor tissue analyses were published in Science Advances. The team showed that disrupting P2Y2 led to near‑complete loss of mutant EGFR and tumor regression in models, and noted P2Y2’s cell‑surface location renders it more accessible to drugs than intracellular degradation machinery. Authors proposed P2Y2 as a tractable target to overcome resistance in EGFR‑mutant, drug‑resistant lung cancers, particularly prevalent in Southeast Asian patient groups.