We have previously shown that P. falciparum malaria parasites with loss-of-function mutations in the haloacid dehalogenase, HAD1 (PF3D7_1033400), have elevated levels of MEP pathway metabolites, which confers FSM resistance [half maximal effective concentration (EC50) of 4.63 ± 0.46 μM (compared to 0.88 ± 0.05 μM for wild-type (WT) parasites)] [21]. The gene discussed is HADH; the disease is malaria.