Syncytia formation is driven by interactions of surface expressed HIV-1 envelope glycoprotein with CXCR4 and contributes substantially to cell death observed in HIV infection; thus, a decrease in syncytia formation in the JunB KO 1–6 cells would implicate a role for CXCR4 in our observed phenotype. The gene discussed is CXCR4; the disease is HIV infectious disease.