The latter influences FPIX chemistry and multiple FPIX-drug interactions in critical ways. Taken together, a more complex, but clearer molecular model for the mechanism of trophozoite CQ resistance is now possible [Paguio M, Cabrera M, Roepe PD, Submitted]. However, importantly, we should not neglect that trophozoite/DV-specific models for CQ resistance are clearly only one part of the story. Other effects of CQ and other layers of CQ resistance need to be elucidated [28] . Other aspects of CQ pharmacology must be present at the ring and schizont stages of P. falciparum development. Additional physiological functions for PfCRT at the ring and schizont stages must also exist and when altered by mutation also cause CQ resistance for these stages. A key question future science group is how are these physiologic functions related to putative ion or osmolyte transport? For ring stages, based on the recent work of Elliot et al. it seems possible, at least in theory, that controlling Hz chemistry is again, at least, part of the explanation [29] . But for schizonts, the answer must be different. Perhaps mutant PfMDR1 and PfNHE further modulate drug resistance in the presence of mutant PfCRT for these stages as well. Their molecular level function can now also be studied using 'yeast-optimized' recombinant proteins and novel drug probes as described for PfCRT, so additional rapid progress is on the horizon.