In spite of the robust effects of ET‐1 on tumor malignancy, its half‐life is 1–2 min, and therefore, its biological effects are totally dependent on the maintenance of a critical concentration brought about by conversion of its precursor, big‐ET‐1, to ET‐1 by the endothelin‐converting enzyme‐1 (ECE1). Here, EDN1 is linked to neoplasm.