In addition to increased OXPHOS, enhanced anaerobic glycolysis (with increased Pgam1, pyruvate kinase M, and Pgk1 expression) has also been described in a lung cancer model with ARID1A loss, where a small-molecule bromodomain and extraterminal protein (BET) inhibitor (JQ1) was successful in treating tumor cells via glycolysis inhibition [393]. The gene discussed is ARID1A; the disease is neoplasm.