Researchers from the Centro Nacional de Investigaciones Oncológicas aimed to identify pathways that contribute to the metabolic reprogramming ability of cancer cells upon resistance to ataxia-telangiectasia-mutated (ATM) inhibition. Metabolism-centered CRISPR screening identified Kelch-like ECH-associated protein 1 (KEAP1), which is an oxidative stress sensor that controls the Nrf2-regulated antioxidant pathway, as a key factor involved in desensitizing cancer cells to ATM inhibition.