By using stattic, which inhibited the phosphorylation of STAT3 at the Y705 position, we found that Y705-STAT3 negatively regulated tumor cell intrinsic pro-metastatic functions of CSC enrichment and EMT, while inducing TME-related pro-metastatic functions, namely the release of CXCL8 (IL-8)—which is a strong inflammatory chemokine playing causative roles in promoting breast cancer progression, partly through the recruitment of deleterious neutrophils to tumors [36,37]—and expression of the inhibitory immune checkpoint PD-L1. This evidence concerns the gene STAT3 and breast cancer.