Indoor-resting anopheline mosquitoes were collected from Obuasi, Ghana, and were identified morphologically and by PCR as Anopheles funestus Giles. Wild-caught females were induced to lay eggs. Samples of F1 progeny from each family were divided into cohorts and were either exposed to DDT and permethrin or were stored for biochemical analysis. Bioassay data by family show evidence of DDT and pyrethroid resistance in the parent A. funestus population. The sodium channel gene of DDT survivors and DDT-susceptible individuals was PCR amplified and sequenced to determine whether any kdr-type mutations were present. Molecular analysis of the IIS5-IIS6 segment of the sodium channel gene gave no indication of any kdr-type mutations associated with resistance phenotypes. Biochemical analysis suggests that DDT and pyrethroid resistance may be metabolically mediated, although there were no clear correlations between enzyme levels/activities and insecticide resistance across families. Furthermore, an altered acetylcholinesterase conferring carbamate resistance was evident. These results can be used to plan an effective malaria control strategy in the Obuasi region.