MLXIPL (MLX interacting protein like), also known as ChR7 (carbohydrate-responsive element binding protein), is a glucose-responsive transcription factor that serves as a key regulator of hepatic carbohydrate and lipid metabolism. MLXIPL functions primarily as a transcriptional activator that senses intracellular glucose and carbohydrate levels, controlling the expression of de novo lipogenesis (DNL) genes including fatty acid synthase, acetyl-CoA carboxylase, and ATP citrate lyase 1. The protein binds to E-box DNA sequences and can be activated by reductive stress (elevated NADH/NAD+ ratios), with this activation representing a critical mechanism linking glucose sensing to lipogenic gene expression 2. MLXIPL plays a central role in systemic metabolic homeostasis. Its dysregulation contributes to nonalcoholic fatty liver disease (NAFLD) and type 2 diabetes development through excessive conversion of carbohydrates to triglycerides 1. In response to high carbohydrate or sugar diets, MLXIPL activation increases hepatic lipogenesis and influences branched-chain amino acid metabolism 3. Genetic variants in MLXIPL are associated with differential responses to Mediterranean diet interventions and modifications of cardiometabolic risk factors including insulin sensitivity and glucose homeostasis 4. Additionally, MLXIPL deletion is implicated in Williams syndrome pathophysiology, though its specific clinical contributions require further investigation 5. MLXIPL represents a promising therapeutic target for metabolic disease prevention and treatment.