Research on ACSL3 and the cancer-immune microenvironment has shown that ACSL3 not only increases the fibrosis of PDAC by increasing PAI-1 (a profibrotic TGF-β–responsive gene) secretion from tumor cells but also drives the tumor microenvironment toward immunosuppression, which predicts poor PDAC patient survival [46]. This evidence concerns the gene TGFB1 and neoplasm.