Consistently, KRAS-mutant NSCLC cell lines with co-inactivation of LKB1 and KEAP1 display increased sensitivity to GLS inhibitors compared to other cell lines (104), indicating that targeting glutaminolysis in KRAS-mutant NSCLC with co-inactivation of LKB1 and KEAP1 holds promise as a therapeutic strategy. The gene discussed is KEAP1; the disease is non-small cell lung carcinoma.