As Sotorasib is approved for use in patients who became resistant to first line therapies, a patient population which will be enriched with KEAP1 and NFE2L2 mutant tumours, we were interested in understanding how Sotorasib may interact with KEAP1-NRF2 signaling (Fig. 1a) Through this approach, we found that electrophilic KRASG12C inhibitors function as classical inducers of the NRF2-dependent antioxidant and xenobiotic responses. This evidence concerns the gene KEAP1 and neoplasm.