The different mechanisms of action of ChT may result in a broad spectrum of clinical, pathological and radiological hepatic injuries, including diffuse and/or focal hepatopathy, such as acute or chronic hepatitis, steatosis, fibrosis, pseudocirrhosis, sinusoidal changes (i.e., sinusoidal obstruction syndrome [SOS], centrilobular sinusoidal dilatation or peliosis) and nodular hyperplasia (Fig. 14) (i.e., nodular regenerative hyperplasia or FNH-like lesions). This evidence concerns the gene SLC5A7 and hepatic veno-occlusive disease.