The results we present are the first to demonstrate a clear role for SP1 in the regulation of PKCβII expression in CLL cells, and we suggest that access of SP1 to the promoter of PRKCB likely results both from a chromosome landscape that is permissive of gene transcription and from VEGF-mediated inhibition of the suppressive effects of STAT3. This evidence concerns the gene PRKCB and B-cell chronic lymphocytic leukemia.