Pre-clinical experiments have demonstrated T cell-dependent control of PDA growth in mice receiving the selective CXCR4 antagonist, AMD3100, in combination with anti-PD-L1 (Feig et al., 2013). We treated freely feeding, weight-stable pre-cachectic PDA-bearing mice for 6 days with a continuous infusion of AMD3100 or PBS, in combination with anti-PD-L1 or isotype control antibody, in the context of subcutaneous pellets releasing corticosterone at a rate of 0.02 mg/hr or placebo control pellets. The gene discussed is CXCR4; the disease is Patent ductus arteriosus.