SLC6A14 is a Na+/Cl−-dependent amino acid transporter that mediates uptake of neutral and cationic amino acids (particularly leucine and lysine) across the intestinal epithelium and other cell types 1. The transporter also accepts non-alpha amino acids like beta-alanine and carnitine species 23. Beyond its classical absorptive function, SLC6A14 has emerged as a multifactorial disease modifier. In cystic fibrosis, it exhibits pleiotropic effects on meconium ileus occurrence, lung disease severity, and P. aeruginosa infection timing 4. In ulcerative colitis, SLC6A14 upregulation correlates with disease markers and promotes NLRP3 inflammasome-mediated pyroptosis in intestinal epithelial cells, while reducing SLC6A14 suppresses inflammatory responses 56. Mechanistically, SLC6A14-mediated glutamine uptake supports macrophage IL-1β secretion through histone phosphorylation pathways 7. In cancer contexts, elevated SLC6A14 promotes glutamine-driven oxidative phosphorylation and cancer stemness in early-onset breast cancer 8, facilitates gemcitabine resistance and immune evasion in pancreatic cancer via mTOR/NF-κB signaling 9, and supports bladder cancer progression through histone lactylation 10. These findings identify SLC6A14 as a therapeutic target across inflammatory and malignant diseases.