Furthermore, transplantation of defined microbial communities with genetically human commensals with engineered microbial cutC gene (an enzymatic source of choline-to-trimethylamine transformation) into germ-free mice is sufficient to transmit trimethylamine-N-oxide production, heighten cerebral infarct size, and lead to functional impairment [28]. The gene discussed is CUTC; the disease is brain infarction.