The concept of toxicant-associated liver disease (TALD) has recently emerged linking exposure to pollutants to the development of chronic liver diseases (CLD) including fibrosis. Among such pollutants, ligands of the Aryl hydrocarbon Receptor (AhR), a transcriptional factor involved in detoxification processes, have been suspected to trigger multiple mechanisms (oxidative stress, epithelial and mesenchymal transition) associated with the occurrence of such pathologies. However, AhR knockout-mice also could develop liver fibrosis, an observation which might first be described as a paradox. In this review, we will present the different mechanisms linking AhR ligands and CLD and provide a hypothesis to solve this paradox.