Another strategy for converting CAFs was suggested in a recent study which showed that targeting Pin1, which is a proline isomerase involved in multiple oncogenic pathways, significantly attenuated the expression of α-SMA in myCAFs as well as of inflammatory cytokines (IL-6, LIF, CXCL12) in iCAFs in the tumor stroma of a PDAC mouse model, which was accompanied by a significant increase in the sensitivity of tumors to chemotherapeutics [66]. This evidence concerns the gene ACTA1 and neoplasm.