A study published in *Nature* (2014) reveals that tumour-derived lactic acid plays a critical role in the functional polarization of tumour-associated macrophages (TAMs). Tumour cells produce lactic acid through aerobic or anaerobic glycolysis, which signals macrophages to adopt an M2-like phenotype, characterized by the expression of vascular endothelial growth factor (Vegf) and arginase 1 (Arg1). This process is mediated by hypoxia-inducible factor 1α (HIF1a), which stabilizes under normoxic conditions. Lactic acid induces Vegf and Arg1 expression in macrophages, promoting tumour growth by facilitating neovascularization and providing substrates for cancer cell proliferation. The study used syngeneic murine tumour models, including Lewis lung carcinoma (LLC) and B16-F1 melanoma, to demonstrate that TAMs express high levels of Vegf and Arg1, consistent with their tumour-promoting role. Lactic acid, a by-product of glycolysis, is shown to induce M2-like polarization of TAMs, with the expression of M2 markers such as Fizz1, Mgl1, and Mgl2. The findings suggest that lactic acid acts as a key signal for macrophage polarization in tumours, potentially evolving from a homeostatic function in normal tissues. The study also highlights the role of HIF1a in mediating this process and demonstrates that TAMs contribute to tumour progression through their metabolic and functional activities. The research underscores the importance of lactic acid in tumour-macrophage communication and its potential as a therapeutic target in cancer treatment.A study published in *Nature* (2014) reveals that tumour-derived lactic acid plays a critical role in the functional polarization of tumour-associated macrophages (TAMs). Tumour cells produce lactic acid through aerobic or anaerobic glycolysis, which signals macrophages to adopt an M2-like phenotype, characterized by the expression of vascular endothelial growth factor (Vegf) and arginase 1 (Arg1). This process is mediated by hypoxia-inducible factor 1α (HIF1a), which stabilizes under normoxic conditions. Lactic acid induces Vegf and Arg1 expression in macrophages, promoting tumour growth by facilitating neovascularization and providing substrates for cancer cell proliferation. The study used syngeneic murine tumour models, including Lewis lung carcinoma (LLC) and B16-F1 melanoma, to demonstrate that TAMs express high levels of Vegf and Arg1, consistent with their tumour-promoting role. Lactic acid, a by-product of glycolysis, is shown to induce M2-like polarization of TAMs, with the expression of M2 markers such as Fizz1, Mgl1, and Mgl2. The findings suggest that lactic acid acts as a key signal for macrophage polarization in tumours, potentially evolving from a homeostatic function in normal tissues. The study also highlights the role of HIF1a in mediating this process and demonstrates that TAMs contribute to tumour progression through their metabolic and functional activities. The research underscores the importance of lactic acid in tumour-macrophage communication and its potential as a therapeutic target in cancer treatment.