We investigated whether the endotoxin-producing pathobiont E. cloacae B29 induces NAFLD in C3H/HeN GF mice with or without TLR4 deficiency to decipher if B29 acts through the LPS-TLR4 signaling pathway and whether its capacity to induce NAFLD is a common phenomenon independent of the genetics of the mouse lines. This evidence concerns the gene TLR4 and metabolic dysfunction-associated steatotic liver disease.