Ultimately, genetics and cell physiology can only take us so far, and cannot fully resolve speculation regarding substrates of PfCRT or define the thermodynamics and kinetics of any proteinmediated transport. Elucidating the remaining questions will require detailed molecular studies with PfCRT, PfMDR1, PfNHE and perhaps other proteins yet to be described. However, the P. falciparum genome is anomalously AT rich, and some genes (including pfcrt) can have significant stretches of AT content that are 80% or more. These do not translate well in convenient heterologous systems such as bacteria or yeast. In fact, in the case of pfcrt and pfmdr1 they do not translate at all. That is unfortunate, since techniques and strategies for defining transporter function have been elegantly laid out in bacteria and yeast model systems for the past four decades. Proteoliposomes, kabackosomes, Goffeau membranes, and Menendez phase separated yeast vesicle preparations would all prove incredibly useful for defining the molecular mechanism of CQ resistance, if only pfcrt cDNA could be expressed in either bacteria or yeast.