Preclinically, loss of KEAP1 (which leads to activation of NRF2) has been shown to drive drug resistance by enabling tumor cells to withstand therapeutic stress; consistently, inhibition of KEAP1/NRF2 signaling or adding mTOR inhibitors showed promise in overcoming resistance in KEAP1/STK11 co-mutant KRAS models [56,57]. This evidence concerns the gene KRAS and neoplasm.