Several important subtypes can now be described pharmacologically, genetically and (to some extent) in terms of their physiology and biochemistry. As elucidated in several other reviews there are many parallels between drug resistance in tumor cells versus P. falciparum [6, 8, 23] . A key role for ATP-binding cassette (ABC) proteins was emphasized early on, however, this cannot explain all phenomena [8, 23, 32, 33] . Many reports underscore an important role for ion transport in drug resistance phenomena [34] [35] [36] [37] and it is now generally well accepted that dysregulation of ion transport is likely to be central to multidrug resistance in tumor cells, malarial parasites and some bacteria. This suggests that altered drug accumulation in MDR cells may be due, at least in part, to consequential alterations in pH gradients, volume and/or other biophysical parameters that control diffusion or accumulation of drugs; that signal transduction regulated by ion transport is a key player in resistance (this is certainly now clearly recognized for apoptotic signal transduction vs tumor multidrug resistance); and that the chemistry of drug-target interactions is manipulated via ion transport such that drug activity is then altered (e.g., the special case of highly pH-dependent FPIX-quinoline interactions described earlier).