Pharmacogenomic studies indicate that certain individuals may be at higher risk: pathogenic CFTR variants (e.g., ΔF508 and R117H) impair pancreatic ductal secretion and increase pancreatitis risk; SPINK1 p.N34S variant weakens trypsin inhibition, conferring an approximately 2.8-fold increased risk of elevated pancreatic enzymes and gastrointestinal symptoms during GLP-1RA therapy [60,61]; moreover, rare variants in PRSS1 and CTRC are associated with earlier onset and progression of chronic pancreatitis. This evidence concerns the gene CFTR and pancreatitis.