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Introduction. Aphis pomi (De Geer) has developed resistance to organophosphate and carbamate insecticides, as a result of long-term application of these insecticides in conventional apple orchards. For many years, the only mechanism of resistance identified in aphids was overproduction of insecticide-detoxifying esterases. Materials and methods. Insecticide resistance of A. pomi, collected from two conventional apple orchards (localities of Radmilovac-RA and Bela Crkva-BC) and one organic apple orchard (locality of Surcin-SU), was tested by bioassays and biochemical assays. Results and discussion. Compared with LC50 values for the susceptible population (organic orchard), both populations from the conventional orchards were highly resistant to pirimicarb (234.5 and 52.9 times) and moderately resistant to dimethoate (10.7 and 9.0 times). Increased esterase activity was determined in these two resistant aphid populations. Each of them also produced one esterase isoform more than the susceptible population, when 1-naphthyl acetate was used as a substrate for zymographic detection; when 2-naphthyl acetate was used as a substrate, only one resistant population produced two new esterase isoforms. In one of the resistant populations acetylcholinesterase (AChE) was significantly less inhibited by pirimicarb than in the other resistant population and the susceptible population, which indicates that this population developed another resistance mechanism-Modification of AChE (MACE). Conclusion. Detoxification of insecticides by the metabolic resistance mechanism of esterase enzymes and mechanism of modification of AChE was proven in one aphid population (RA). The other population (BC) has developed only metabolic resistance (enhanced metabolism by esterases), without modification of the insecticide target site (AChE). Development of insecticide resistance was caused by long-term application of acetylcholinesterase inhibitors (organophosphates and carbamates) in these conventio