reported an increase in the expression of genes involved in glutamine metabolism in lung adenocarcinoma cells with the mutations of KRAS, STK11/LKB1 and KEAP1. In fact, KRAS/LKB1/KEAP1 mutant tumors were found to be dependent on glutamine metabolism, unlike KRAS mutated tumors, and consequently they turned out to be sensitive to the glutaminase inhibitor CB-839 in vitro and in vivo (96). Here, STK11 is linked to lung adenocarcinoma.