Using an ethyl carbamate-induced lung carcinogenesis model, Nrf2-ko mice have been shown to be substantially more sensitive than wildtype mice to the early stages of tumourigenesis but, surprisingly, seem to be more resistant to the later stages of lung tumourigenesis than their wildtype counterparts, suggesting that whilst Nrf2-target genes antagonise initiation of chemical carcinogenesis they facilitate the later transformation of benign adenoma to adenocarcinoma that may entail mutation of Kras [103]. Here, NFE2L2 is linked to adenoma.