GM-CSF-treated hCD4/R5/cT1 mouse myeloid-lineage cells developed sustained HIV-1 infection as evidenced by the 2-fold increase in LucR activity detected over 7 days of culture at levels 20–25% of the 3-fold increase in LucR activity observed for GM-CSF-stimulated human monocytes, while the hCD4/R5/cT1 mouse CD4 T cells supported only transient HIV-1 infection at ∼5% of the levels observed after infection of human CD4 T cells (Figure 3B). The gene discussed is CD4; the disease is HIV-1 infection.