Although no study has clearly revealed the direct relationship between TNFRSF12A (TWEAK receptor) and the JAK/STAT pathway in inflammation, it has been demonstrated that TWEAK/Fn14 induces IFNβ and promotes apoptosis in tumor cells via the JAK-STAT pathway, and this process is JAK-dependent [49]. The gene discussed is SOAT1; the disease is neoplasm.