However, a subsequent study revealed that CTSB contributes not only to the activation of trypsinogen within acinar cells but also within infiltrating macrophages, thereby exacerbating pancreatitis through NF-κB nuclear translocation and the production of inflammatory mediators.188 These findings suggest that CTSB inhibitors may act on both acinar cells and macrophage-driven inflammation and that dual-targeted strategies focusing on CTSB and its downstream signaling (e.g., NF-κB) may offer a more comprehensive approach to treatment. The gene discussed is CTSB; the disease is pancreatitis.