In support, depletion of αSMA-positive CAFs in a transgenic mouse model of pancreatic cancer (Ptflacre/+; LSL-KrasG12D/+; Tgfβr2flox/flox) during either non-invasive precursor or PDAC stages of oncogenesis has been shown to enhance the Treg cell population and intra-tumoral hypoxia, leading to a more invasive tumor phenotype [184]. Here, ACTA1 is linked to pancreatic neoplasm.