Other factors secreted within the tumor, such as vascular endothelial growth factor, epidermal growth factor, and platelet‐derived growth factor may also activate STAT3.9, 10 High serum levels of IL‐6 in PCa patients have been implicated in lower survival rates.11 Activation of STAT3 by phosphorylation on the 705 tyrosine or the 727 serine has been observed to be involved in cancer progression and a more aggressive phenotype of PCa.12 However, STAT3 may in certain contexts act as a tumor suppressor 10 and new evidence is emerging showing antioncogenic roles of the STAT3‐IL‐6 pathway in PCa.13 This evidence concerns the gene STAT3 and posterior cortical atrophy.