The gut microbiota produces urease, which transforms urea into ammonia and carbon dioxide. Ammonia has several beneficial roles in host metabolism, but patients with liver disease are unable to process ammonia in the liver, which results in an increase in the systemic levels of ammonia; this leads to neurotoxicity and results in hepatic encephalopathy. Shen et al. engineered the microbiota of mice to express low levels of urease by depleting the endogenous microbiota via the use of antibiotics and polyethylene glycol, followed by gavage of a defined consortium of eight bacterial strains with reduced capacity to produce urease, termed altered Schaedler flora (ASF). This strategy resulted in the establishment of a persistent gut microbiota that displayed reduced levels of ammonia production for up to 80 days. Notably, in murine models of liver injury, ASF transplantation resulted in reduced levels of ammonia, improved cognitive performance and reduced mortality.