As we previously showed that Gprc5a−/− mice with a knock-out of lipocalin 2 (Gprc5a−/−; Lcn2−/−) are more susceptible to nicotine-specific carcinogen-mediated lung cancer development compared to similarly exposed Gprc5a−/− with intact Lcn2, we sought to investigate the microbial evolution following NNK exposure in this mouse model [11]. This evidence concerns the gene GPRC5A and lung cancer.