At the same time, a recent work by Qian and colleagues highlighted the role of lactate as the link between LKB1 metabolic roles and TIME modulation: in murine lung adenocarcinoma models, LKB1 loss resulted in increased glycolysis and enhanced lactate production and export via the monocarboxylate transporter 4; this caused increased M2 macrophage polarization, which in turn resulted in hypofunctional T cells (47). The gene discussed is STK11; the disease is lung adenocarcinoma.