Using gene screening and metabolomics analysis in conjunction with the CRISPR/Cas9 system, Romero et al. showed that cancers with KEAP1 or NRF2 mutations rely on increased glutamine metabolism, providing a rationale for glutaminase inhibitors in the treatment of patients with KRAS/KEAP1 or KRAS/NRF2 mutant lung cancer. The gene discussed is KEAP1; the disease is lung carcinoma.