OATP1B1 and OATP1B3 are transporters that are expressed on the sinusoidal membrane of hepatocytes; they accept a number of therapeutic reagents as their substrates. In vitro and in vivo studies have shown that some drugs inhibit these transporters and cause clinically relevant drug-drug interactions (DDIs). Among these drugs, cyclosporin A markedly increases the plasma concentrations of OATP1B1 substrates. In such cases, the area under the plasma concentration-time curve and the maximum concentration of the affected drugs are increased to a similar degree. Even for OATP1B1 substrates that are metabolized in the liver, the hepatic uptake rate is a determinant of overall hepatic clearance, and the DDIs are partly caused by the inhibition of OATP1B1. Gemfibrozil displays DDIs with some OATP1B1 substrates, although their extent is small. Rifampicin and some HIV protease inhibitors are also OATP1B1 inhibitors. Rifampicin is also an inducer of metabolic enzymes, and although its single coadministration produces an increase in the plasma concentration of the affected drugs, multiple coadministrations may result in reductions in the plasma concentrations of OATP1B1 and CYP3A4 bisubstrates. As a large number of therapeutic reagents are substrates and/or inhibitors of OATP1B1 and OATP1B3, we should be aware of DDIs caused by the inhibition of these transporters.