These findings are consistent with studies in other cancers, including triple-negative breast cancer, where the FGF2/FGFR1 transduction pathway induces the upregulation and secretion of S100A4 [39], with extracellular S100A4 released by tumor or stromal cells acting in an autocrine or paracrine manner by binding to its RAGE receptor, thus promoting cell migration, invasion, and angiogenesis [40,41]. This evidence concerns the gene S100A4 and triple-negative breast carcinoma.