Based on our previous demonstration that GM-CSF markedly increased HIV-1 production by myeloid-lineage cells from JR-CSF/hCycT1 mice which carry as transgenes a full-length infectious JR-CSF provirus and a CD4 promoter/enhancer-regulated human cyclin T1 construct [16], we postulated that GM-CSF treatment would also facilitate productive HIV-1 infection of hCD4/R5/cT1 mouse myeloid-lineage cells. The gene discussed is CSF2; the disease is HIV-1 infection.