Since the primary event involved in the majority of drug-induced cholestasis in vivo is accumulation of bile acids due to inhibition of export transporters such as BSEP, we hypothesized that to further optimize the PCLS to mimic cholestasis induced by accumulation of the bile acids in vivo, the PCLS should be incubated with a non-toxic concentration of a bile acid mix mimicking the portal vein bile acid concentration and composition. The gene discussed is ABCB11; the disease is cholestasis.