CBR4 (carbonyl reductase 4) functions as a β-subunit in the heterotetrameric KAR (3-ketoacyl-ACP reductase) complex, which is essential for mitochondrial fatty acid synthesis (mtFAS) 1. The CBR4 subunit provides NADPH-dependent 3-ketoacyl-ACP reductase activity, reducing 3-oxoacyl-[ACP] to (3R)-hydroxyacyl-[ACP] without chain length preference 1. Additionally, CBR4 exhibits NADPH-dependent quinone reductase activity as a homotetramer, potentially protecting against cytotoxicity from exogenous quinones including 9,10-phenanthrenequinone and various o-quinones and p-quinones 2. The enzyme localizes to mitochondria via a non-cleavable targeting signal 2. CBR4 demonstrates tumor suppressor properties in colorectal cancer by interacting with fatty acid synthase (FASN), promoting its degradation through the ubiquitin-proteasome pathway and inhibiting the mTOR pathway 3. CBR4 expression is reduced in colorectal cancer tissues due to DNMT3B-mediated promoter methylation 3. The enzyme shows regional expression variation in human tissues, with relatively uniform expression across intestinal regions compared to other reductases 4.