Since the depletion of α-SMA-positive CAF worsened the PDAC phenotype and prognosis [14], myCAF was considered as a cancer-restraining CAF, whereas the distinct cluster iCAF was considered as a cancer-promoting CAF because the inflammatory cytokines and other factors secreted by iCAF have been shown to promote PDAC, and also due to the PDAC-suppressing effect of JAK/STAT inhibition, described above [40]. Here, ACTA1 is linked to cancer.