Consistent with the implications of the genetic evidence, we and others have shown that conditional Acvr1b knockout in the pancreases of mice synergized with oncogenic Kras induced pancreatic tumorigenesis [127,128], providing functional evidence that inactivation of the activin signaling pathway in the epithelial compartment promotes tumor development in the early stages of pancreatic tumorigenesis. Here, INHBE is linked to neoplasm.