We previously found that Gprc5a−/− mice, when exposed to tobacco carcinogen, develop accelerated premalignant lesions (hyperplasias and adenomas) compared to wild-type littermates and harbor in their tumors somatic activating mutations in Kras G12D that are highly pertinent to human LUAD in smokers [10,13,14,15]. The gene discussed is GPRC5A; the disease is adenoma.