The ablation of the Acvr1b gene promoted KrasG12D‐mediated tumorigenesis and decreased PDAC survival in mice.[29] Additionally, consistent observations were made by the loss of the Smad4 gene, in mice harboring KrasG12D.[30] However, loss of Acvr1b or Smad4 occurs before KrasG12D‐dependent tumor development.[29, 30] Therefore, the evidence addresses the importance of activin A signaling in tumorigenesis, especially the development of PDAC precursor lesions. Here, SMAD4 is linked to neoplasm.