Specifically, as cancers with pre-existing KEAP1 or NFE2L2 mutations exhibit constitutive NRF2 activation, they will not benefit from NRF2 induction by G12Ci drugs, while in contrast, tumours with wild-type KEAP1-NRF2 will benefit from G12Ci-induced NRF2 activation. Here, KEAP1 is linked to neoplasm.