In preclinical models of pancreatic cancer, JAK inhibitors have been found to inhibit LIF signaling in IL-1-induced inflammatory iCAFs, thereby converting iCAFs to ECM-producing myCAFs, increasing the myCAF-to-iCAF ratio, and promoting ECM deposition, leading to a reduction in cancer cell proliferation and tumor growth [8]. The gene discussed is IL1B; the disease is pancreatic neoplasm.