Vectorial transport of solutes from the sinusoidal space to the canaliculus provides the osmotic driving force for bile formation and is accomplished by various transporters located at the basolateral and canalicular membrane of hepatocytes and cholangiocytes. 1–7 The term “cholestasis” is used to describe conditions associated with decreased bile formation. It is thus easy to appreciate the paradigm that cholestasis results when the ability of the liver to transport solutes into the canaliculus is compromised. Our present understanding of the pathogenesis of cholestasis is based on studies to define the physiologic regulation of various transporters (Fig. 1) and their deregulation in experimental models of cholestasis and patients with cholestatic disorders. 8–11 In addition, studies on the expression of transporters in cholestatic diseases have provided valuable information on the role of specific transporters in the pathogenesis of some of these disorders. It is becoming clear that multiple pathways are involved in the regulation of hepatocellular solute transport and, hence, bile formation.