In another rodent malaria parasite, P. berghei, it was shown that FabG null mutant parasites form normal numbers of oocyst and produce sporozoites1, pointing to a redundant function of FabG—and hence of of FAS—in the oocyst stage and thus a FA acquisition scenario similar to the closely related species P. yoelii. This evidence concerns the gene HSD17B8 and malaria.