Indeed, it was recently reported that a mutated sema3A, that unlike natural sema3A binds directly to the plexin-A4 receptor and not to neuropilin-1, is a better inhibitor of angiogenesis as compared to wild type sema3A and strongly inhibits the progression of pancreatic cancer in mouse models [89]. Here, SEMA3A is linked to familial pancreatic carcinoma.