In obese mice of spontaneous breast tumour remission, ablation of T-cell STAT3 protein or treatment with FAO inhibitors reduced FAO, increased glycolysis and upregulated the function of TEFFs, which inhibited the development of the breast tumours, while PD-1 ligation to CD8+ T cells activated Stat3 to increase FAO, inhibit glycolysis and downregulate the function of TEFFs. The gene discussed is STAT3; the disease is breast neoplasm.