We found that rescue of endogenous CCN1, which was knocked down by shRNA that targeted 3ʹ-untranslated regions (UTRs), by exogenously transduced lentiviruses that harbored WT CCN1 restored macrophage infiltration in vitro and in vivo, increased the tumor size, and reduced animal survival, but not the empty vector control or CCN1 mutants defective for integrin binding (Fig. 7g–k, Additional file 1: S7c–g). The gene discussed is CCN1; the disease is neoplasm.