We speculate that similar pathophysiological changes may occur in the lungs of IPF patients, where bile acid metabolic imbalance may lead to ROS generation, subsequently activating pro-fibrotic enzymes such as lysyl oxidase (LOX), exacerbating collagen cross-linking (in synergy with MMP/TIMP imbalance), and inducing apoptosis.Despite these insights, significant gaps remain in understanding the precise role of BAAT in IPF. Here, LOX is linked to idiopathic pulmonary fibrosis.