Briefly, the primary B16-F10 tumors were established on the left flank of mice, and these mice either were treated with RdB/IL12/GMCSF-RLX monotherapy (5 × 107PFU/dose) or in combination with αPD-1 as described in Fig. 2, and mice that remained in complete tumor regression at day 51 were rechallenged with B16-F10 cells on the opposite flank to establish the recurrent tumors. The gene discussed is CSF2; the disease is neoplasm.