Likewise, the constitutively active form of K-RAS (G12D) was found to promote NRF2 transcription and chemoresistance through the MEK/ERK pathway in NSCLC cells and in a murine model of lung cancer, being the effects at least partially reverted by coadministration of the NRF2 inhibitor Brusatol [236]. This evidence concerns the gene KRAS and lung carcinoma.