Vasostatin‐1, but not hCgA1–373, could inhibit CLL progression in the xenograft model, suggesting that the N‐terminal domain contains a site activated by proteolytic cleavage, and that the C‐terminal region is crucial for CgA activity.183 It is therefore possible that CgA and its fragments contribute to regulate leukemic cell trafficking and tissue infiltration in patients with CLL. This evidence concerns the gene CGA and B-cell chronic lymphocytic leukemia.