In the breast cancer context, it has been shown that increased stiffness/density of the extracellular matrix around the tumor as a result of altered collagen deposition during cancer progression shifted the balance of PRLR signaling from JAK2/STAT5 to other pathways including ERK1/2 and AKT pathways through a Focal adhesion kinase-dependent mechanism [54,55]. This evidence concerns the gene STAT5A and neoplasm.