Additionally, both in vitro and in vivo experiments demonstrated that the PHGDH inhibitor or JAK1 inhibitor enhanced the chemotherapy sensitivity of CXCL7-overexpressing tumors (Fig. 5H–J), indicating that CXCL7 upregulates PHGDH via STAT1, thereby activating serine synthesis and mediating tumor resistance to chemotherapy. The gene discussed is JAK1; the disease is neoplasm.