A model for the mechanism on transcription of human VEGF gene by HIF-1α associated with STAT3 in CLL B cells. Expression of HIF-1α in CLL B cells is stabilized due to a reduced level of pVHL, at least in part, through posttranscriptional modification by the overexpressed miR-92-1. Stabilized HIF-1α localizes in the nucleus and heterodimerizes with HIF-1β. Active HIF-1 heterodimer then forms a complex with constitutively active STAT3 and p300 by physical association. In CLL B cells, this active transcriptional complex binds the human VEGF promoter through the HIF-1– and STAT3-specific DNA-binding elements present on the promoter. DNA-bound HIF-1/STAT3/p300 complex then recruits RNA polymerase II transcription machinery at the promoter to transcribe the VEGF gene.