The mechanism by which MRP2 influences the risk of KTD in these patients is not well understood. Three hypotheses may be considered. First, tenofovir could be excreted less efficiently by tubular cells in ABCC2 −24C homozygotes, as suggested elsewhere [19]. Increased intracellular concentrations of tenofovir within epithelial tubular cells could be deleterious. However, tenofovir metabolites have not been found to be increased in peripheral blood mononuclear cells of carriers of genotype CC at ABCC2 [28], although this may be accounted for by differences in the nucleotide pool equilibrium and metabolism between blood cells and epithelial tubular cells.