Notably, PSCs differentiated in two CAF subpopulations, preferentially standing in distinct locations respect to cancer organoids: α-smooth muscle actin (αSMA)high IL-6low myofibroblastic CAFs (myCAFs) directly interacting with cancer cells and peripheral αSMAlow IL-6high inflammatory CAFs (iCAFs) scattered in areas distant from PDAC cells able to promote tumorigenesis through inflammatory cytokine production. This evidence concerns the gene ACTA1 and cancer.