Acetate binds to the G protein‐coupled receptor 43 of liver cells, activates GPR43, and inhibits the IL‐6/JAK1/STAT3 signaling pathway, thereby suppressing NAFLD‐HCC formation.[26] Our study, which has been causally validated at the genomic level and in a mouse model of DSS‐induced colitis, confirms that B. pseudolongum promotes the production of secondary bile acids in the intestine, in particular the levels of HDCA and 12‐KCAC, to alleviate colitis. Here, STAT3 is linked to metabolic dysfunction-associated steatotic liver disease.