Our results using the selective kinase inhibitor supported a canonical kinase-dependent role of CD167a/DDR1 in activating Stat3 in our bladder cancer metastasis models (Fig. 6b, c), highlighting the significance of organ-site specificity, postulating discrete canonical and non-canonical CD167a/DDR1 signaling in different tissue types. This evidence concerns the gene STAT3 and urinary bladder carcinoma.