Kaul and colleagues used a spontaneous mammary tumour virus promoter–polyoma middle T antigen (PyMT) breast cancer mouse model and found that Slit2 promoted BMDMs polarization towards an anti-tumour phenotype and enhanced the anti-tumour immune response by increasing glycolysis and reducing FAO in BMDMs via the mTOR signalling pathway. The gene discussed is SLIT2; the disease is neoplasm.