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). This evidence concerns the gene JUN and neoplasm.