All these findings suggest that hyper-activation of STAT3 measured by immunohistochemistry likely represent a surrogate biomarker of basal-type UBC with an active pro-inflammatory environment and high TAN density; however, STAT3 blockade on tumor cells, as recently proposed [40], is likely insufficient to dampen TAN recruitment, since STAT3-independent pathways could also be operative in this system. Here, STAT3 is linked to neoplasm.