Tumors in the proximal-proliferative subtype have variable histology and commonly display mutations and copy number alterations in KRAS and STK11. In contrast, lung adenocarcinomas with primarily solid architecture and enrichment for TP53 and NF1 mutations and p16 methylation typically cluster in the proximal-inflammatory subtype [8, 15]. The gene discussed is KRAS; the disease is lung adenocarcinoma.