B-cell chronic lymphocytic leukemia (CLL) is characterized by asymmetrical proliferation and apoptosis of leukemia cells co-expressing the CD5 and CD19 antigens [1, 2], and several chromosomal abnormalities, including del(13q), del(11q), del(17p), and trisomy 12, are detected in most, but not all, cases. However, in almost all patients, regardless of their cytogenetic abnormalities, clinical characteristics, disease stage, or treatment status, signal transducer and activator of transcription 3 (STAT3) is constitutively phosphorylated on serine 727 residue [3, 4]. Phosphoserine STAT3 shuttles to the nucleus, binds to DNA, and activates genes known to be activated by phosphotyrosine STAT3 in other cell types . Furthermore, unphosphorylated STAT3, detected at high levels in CLL cells, constitutively activates the transcription factor nuclear factor κB , which is known to induce the production of several pro-inflammatory cytokines and activate survival pathways.
STAT3-induced transcription of protein-coding genes has been extensively studied in normal and neoplastic tissues. However, protein-coding genes comprise only 3% of the human genome  and only scant data are available on the role of STAT3 in the transcription of non-protein-coding genes. Although approximately 1000 microRNAs (miRs) collectively regulate more than 30% of protein-coding genes , little is known about miR gene transcription. Iliopoulos et al. found that STAT3 activates the transcription of miR-21 and miR-181b-1, thereby inducing a stable transformed state in cancer cell lines .
Because STAT3 is constitutively activated in CLL cells and recent data demonstrated a global deregulation of the miR network in CLL,  we hypothesized that STAT3 affects the expression of miRs in CLL cells. Therefore, we analyzed publicly available data to determine whether STAT3 binds to miR promoters, and studies the effect of STAT3 on miR expression in CLL cells.