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Therefore, understanding the mechanism is key before considering off-label use

For clinicians, this study challenges the long-standing habit of avoiding GLP-1 drugs in patients with previous pancreatitis

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These divergent results may be explained by impaired Toll-like receptor 4 (TLR4) (25, 53) signaling due to disruption of PAR2 heterodimer formation in the complete PAR2 knockout, whereas selective abrogation of PAR2 cleavage is known to preserve proinflammatory responses but abolishes interferon responses downstream of TLR4 signaling in innate immune cells (54, 55)

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