TBCE and steatosis: Depletion of KCs by treatment with liposomal clodronate [48], gadolinium chloride [49], or by a unique conditional ablation system mediated by the diphtheria toxin receptor [50] has evidenced the crucial role of KCs in hepatic damage provided by attenuating hepatotoxicity in terms of steatosis, inflammation, necrosis, and collagen content in animals [43].