GPAM (Glycerol-3-phosphate acyltransferase, mitochondrial) is a mitochondrial outer membrane-associated acyltransferase and one of the key rate-limiting enzymes involved in triglyceride biosynthesis, primarily expressed in metabolic tissues including the liver and adipose tissue ^[1-2]. GPAM participates in triglyceride and phospholipid synthesis, lipid storage, and energy metabolism regulation, and is closely associated with mitochondrial homeostasis and lipid metabolic reprogramming ^[2-3]. Studies have shown that aberrant GPAM expression or dysfunction is associated with the pathogenesis of metabolic disorders, including Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD), Metabolic Dysfunction-Associated Steatohepatitis (MASH), obesity, and insulin resistance. Therefore, GPAM is considered a potential therapeutic target for metabolic diseases, and studies on GPAM inhibitors and related mechanisms have been conducted ^[3-4]. The huGPAM mouse is a humanized model generated by replacing the sequences from the start codon to downstream of the 3'UTR of the mouse Gpam gene with the sequences from the start codon to downstream of the 3'UTR of the human GPAM gene. This model can be used for in vivo pharmacodynamic and safety evaluation of GPAM-targeted candidate therapeutics and is also applicable for studies of the pathogenesis and progression of metabolic disorders, including Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD), Metabolic Dysfunction-Associated Steatohepatitis (MASH), obesity, and lipid metabolism disorders, as well as lipid metabolic regulatory networks and combination therapeutic strategies.