Using transcriptional profiling, three robust subtypes of nonsquamous non–small cell lung cancer were defined, independently of initiating oncogenic driver events. Subtype-specific differential sensitivity to MEK1/2 inhibitors was reported and an interaction between the mucinous subtype, STK11/LKB1 genomic alterations, and inferior clinical outcomes with atezolizumab in the OAK clinical trial was identified.

See related article by Daemen et al., p. 1162

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