The notion that myofibroblasts have tumor-restraining effects was suggested by the study that depletion of proliferating αSMA+ myofibroblasts in a αSMA-tk (thymidine kinase) transgenic mice with ganciclovir resulted in undifferentiated PDAC and decreased survival35 of the mice, suggesting that αSMA+ fibroblasts may restrain tumor progression. Here, ACTA1 is linked to neoplasm.