These mechanistic investigations revealed interactions of β1-integrin with several factors such as focal adhesion kinase (FAK), urokinase-type plasminogen activator receptor (uPAR), extracellular signal-regulated kinase (ERK), and epidermal growth factor receptor (EGFR), all of which influence tumor microenvironment and have been implicated in breast cancer progression [81–88]. This evidence concerns the gene PLAUR and breast carcinoma.