QPRT (quinolinate phosphoribosyltransferase) is a key enzyme in the de novo NAD+ biosynthetic pathway from L-tryptophan, catalyzing the conversion of quinolinic acid to nicotinic acid mononucleotide 1. As a bottleneck enzyme in this pathway, QPRT activity directly influences cellular NAD+ levels and metabolic homeostasis 1. Mechanistically, QPRT expression is regulated by β2-adrenergic signaling in hepatocytes 2 and is subject to post-transcriptional regulation via m6A methylation 3 and miRNA-mediated control 4. The enzyme's activity diverts kynurenine metabolism toward NAD+ synthesis rather than kynurenic acid accumulation, maintaining mitochondrial function and immune cell energy metabolism 2. Clinically, reduced QPRT expression associates with impaired immune surveillance and disease progression across multiple contexts. Chr16 psychological stress suppresses QPRT in hepatocytes, reducing NAD+ synthesis and hepatic CD8+ T cell function, thereby accelerating liver cancer progression 2. In breast cancer, elevated QPRT expression correlates with worse overall survival, disease-free survival, and recurrence-free survival, particularly in HER2+ and triple-negative subtypes 56. LAT1-mediated L-tryptophan uptake upregulates QPRT to promote NAD+-dependent metabolic reprogramming driving breast cancer progression and chemoresistance 7. Conversely, QPRT reduction via therapeutic interventions (NAD+ supplementation, LAT1 inhibition) restores immune function and chemosensitivity 27, positioning QPRT as both a prognostic biomarker and therapeutic target.