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Cheung and colleagues demonstrate that amplified CRKL can function as a driver oncogene in lung adenocarcinoma, activating both RAS and RAP1 to induce mitogen-activated protein kinase signaling. In addition, they show that CRKL amplification may be another mechanism for primary or acquired resistance to epidermal growth factor receptor kinase inhibitors.

CRKL as a Lung Cancer Oncogene and Mediator of Acquired Resistance to EGFR Inhibitors: Is It All That It Is Cracked Up to Be?