Our findings support and add greater relevance to previous studies demonstrating that, in normoxic conditions, but even more so in hypoxic conditions, the alliance between HIF-1α and mutp53 signals potentiates the release of soluble factors that remodel the ECM and affect stromal cell activity, thereby enhancing tumor growth and metastatic potential in breast cancer [36, 37]. This evidence concerns the gene HIF1A and breast carcinoma.