Prior work from our group and others have revealed that inflammatory CAF (iCAF)-derived IL-6 engages in tumor-permissive crosstalk by activating STAT3 signaling with tumor cells (Nagathihalli et al., 2016), and that the CAF-tumor cell IL-6/STAT-3 signaling axis is a central mediator of chemoresistance in PDAC (Hosein et al., 2020; Dosch et al., 2021). The gene discussed is STAT3; the disease is neoplasm.