Similar levels of PR were found in all tumor samples, indicating that the antiproliferative effects of the blockade of AP-1 activation, and consequently of the assembly of the AP-1/Stat3/PR/ErbB-2 transcriptional complex, are not due to regulation of PR expression levels, but to the blockade of the assembly of PR nonclassical transcriptional complexes (Figure 6G). The gene discussed is STAT3; the disease is neoplasm.