CUTC is an intracellular copper-binding protein involved in copper homeostasis. It can bind one Cu(1+) per subunit and functions through protein tetramerization 1. In human cells, CUTC maintains intracellular copper balance; silencing hCutC increases cellular sensitivity to copper loads and induces apoptosis through mitochondrial dysfunction and DNA fragmentation, despite unchanged total cellular copper levels 1. Bacterial CutC (choline trimethylamine-lyase) has distinct roles in microbial metabolism. As a glycyl radical enzyme, it cleaves choline to produce trimethylamine (TMA) and acetaldehyde 2. Choline binding triggers conformational changes in bacterial CutC structure 2. This bacterial TMA production is clinically significant: TMA is converted hepatically to trimethylamine-N-oxide (TMAO), a proatherogenic metabolite. Elevated TMAO associates with abdominal aortic aneurysm incidence and growth 3, and CutC-expressing commensals (particularly Lachnoclostridium and Clostridium species) promote atherosclerosis development 4. Microbial cutC-dependent TMAO production enhances platelet reactivity and thrombosis potential 5. Urinary TMAO levels correlate with fecal cutC abundance and specific bacterial taxa 6. CUTC variants also associate with hair curl phenotype 7, suggesting broader physiological roles beyond copper homeostasis and bacterial metabolism.