In this sense, it has been shown that the availability of Ca2+ plays a determining role in the development of an invasive phenotype in breast cancer cells with pleural metastasis (MDA-MB-468), which, after having been subjected to the intracellular chelation of Ca2+, experienced a pronounced inhibition in the phosphorylation of STAT3, restricting the EMT induced by epidermal growth factor (EGF) by significantly repressing the transcriptional expression of mesenchymal markers such as N-cadherin, Twist, and the CD44/CD24 ratio, and at a translational level, to the vimentin protein. This evidence concerns the gene VIM and breast carcinoma.