Consistent with this effect, in a genetic mouse model of non-small cell lung cancer (NSCLC) driven by a glycine to aspartate mutation (G to D) in the K-Ras oncogene (K-RasG12D), AHR−/− mice developed more tumors than their AHR+/+ counterparts and featured increased stem cell populations characterized by the expression of pluripotency markers such as MYCC, SOX2, and NANOG, together with the increased expression of progenitor cell markers [105]. This evidence concerns the gene KRAS and non-small cell lung carcinoma.