Moreover, in lung adenocarcinoma tumors co-occurring KEAP1 mutations and STK11/LKB1 loss lead to metabolic reprogramming (glutamine metabolism), activating the pentose phosphate pathway and the tricarboxylic acid (TCA) cycle to maintain redox balance, suggesting a glutaminase inhibitor as a possible treatment strategy [56]. The gene discussed is STK11; the disease is lung adenocarcinoma.