The main purpose of this study is to provide essential information regarding the molecular basis of insecticide resistance and to report candidate genes which are responsible for resistance in insects/pests. There are two basic resistance mechanisms existing in pests, i.e., target site resistance and metabolic resistance. During resistance of target site, the specific binding site of an insecticide is modified (mutated) and/or lost, which makes the target site incompatible for activation. Mutation occurs in most common pest (Myzus persicae, Musca domestica and Drosophila melanogaster) target regions, i.e., subunits like nicotinic acetylene choline receptors (nAChRs), knock-down resistance (KDR) etc. Due to these mutations, insecticides are unable to bind into the target region, resulting in loss of binding affinity. Furthermore, in metabolic resistance over production of enzymes occurs which break down (detoxify) insecticides and resulting resistance of pests. The amplification of metabolic enzymes, i.e., Cytochromes p450 monooxygenase, hydrolyses, and Glutathione S-transferase play a central role in evolving metabolic resistance. Various successful approaches are used to combat pests resistance such as insecticides, bio-pesticides and biological control agents. However, some of these strategies have certain limitations such as contamination of the environment, while others possess a low capacity in management of pests. Recent studies have highlighted some novel mechanisms of insecticide resistance that are part of the ongoing efforts to define the molecular basis of insecticide resistance in insect species.