BAAT (bile acid-CoA:amino acid N-acyltransferase) catalyzes the conjugation of bile acids with taurine and glycine, a critical step in bile acid metabolism occurring primarily in hepatocytes 1. Over 95% of circulating bile acids are N-acyl amidates with these amino acids [UniProt]. This conjugation promotes bile acid and cholesterol secretion into bile and enhances their detergent properties in the intestine, facilitating lipid and vitamin absorption [UniProt]. BAAT also functions as an acyl-CoA thioesterase, regulating intracellular free fatty acid levels through hydrolysis of long- and very long-chain acyl-CoAs [UniProt]. Mechanistically, BAAT-mediated bile acid conjugation is essential for early postnatal development; Baat knockout mice exhibit reduced growth, altered hepatic lipid storage, and microbiome changes during early life 2. The balance between BAAT-catalyzed conjugation and microbial deconjugation influences gastrointestinal inflammation severity 3. Disease relevance includes familial hypercholanemia 3, caused by BAAT dysfunction [NCBI Summary]. Additionally, BAAT inhibition enhances anti-tumor immunity in hepatocellular carcinoma by reducing immunosuppressive bile acid accumulation and sensitizing tumors to anti-PD-1 therapy 4. Clinical applications include modulating BAAT expression to treat cholestasis 1 and potentially improving cancer immunotherapy outcomes.