The authors further went on to develop a compound, SD1, consisting of the SEMA domain of human PlexinD1 protein to act as a ligand trap to sequester SEMA3E and demonstrated that sequestering SEMA3E triggered the death of PlexinD1-expressing cancer cells in vitro, thereby demonstrating the therapeutic potential of directly targeting the SEMA/Plexin axis [31]. Here, SEMA3B is linked to cancer.