Eight populations of Anopheline mosquitoes showing resistance to one or more insecticide were investigated. Anopheles albimanus , with a Y-linked translocation of a resistance gene, showed broad spectrum organochlorine, organophosphate and carbamate resistance in the males, but only dieldrin resistance in the females. Synergist studies suggest that the translocated gene codes for an altered acetylcholinesterase as the basis of resistance. In An. arabiensis from Sudan synergist studies indicate a kdr-like gene producing DDT and permethrin resistance and an additional DDT-dehydrochlorinase mechanism. Malathion and phenthoate resistance in this species are inherited as a single gene, which appears to produce a qualitative change in a carboxylesterase enzyme. An. atroparvus from England was DDT resistant due to a DDT-dehydrochlorinase mechanism. An. atroparvus from Spain with broad spectrum organophosphate and carbamate resistance, all dependent on a single gene or several closely linked genes, possessed an altered acetylcholinesterase which always segregated with resistance. There was also an oxidase mediated propoxur detoxication mechanism in this population. Three An. stephensi populations from Iraq, Iran and Pakistan were resistant to malathion and phenthoate. A carboxylesterase mediated resistance mechanism is indicated in all three populations from synergist studies. In the Pakistani An. stephensi enzyme assays indicate a qualitative change in a carboxylesterase enzyme rather than a quantitative change. Metabolite production studies supported the supposition of a carboxylesterase mediated resistance mechanism: Fenitrothion resistance was found in An. stephensi from Iraq, it was not connected with the malathion resistance mechanism. An. gambiae from Nigeria showed DDT and permethrin resistance. DDT-dehydrochlorinase and a kdr-like mechanism are indicated as the cause of resistance on the basis of synergist studies.