In our study, we found that SGLT2 was overexpressed at the protein level in osteosarcoma, and we demonstrated that the SGLT2 inhibitor significantly inhibited osteosarcoma tumor growth and induced infiltration of immune cells in vivo by upregulating STING expression, which could be contributed to the suppression of AKT phosphorylation (Fig. 8). The gene discussed is STING1; the disease is osteosarcoma.